Array ( [0] => Array ( [ArticleId] => 96 [Create_Time] => 2021-01-25 [zipUrl] => https://www.explorationpub.com/uploads/zip/202108/20210826040031.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10041/10041.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10041/10041.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10041/10041_cover.png [JournalsId] => 7 [Title] => Science plus technology to address challenges in determining the efficacy of neuroprotective/neurorestorative therapies [Abstract] => [AbstractComplete] => [Names] => Rafael Franco [CName] => RafaelFranco, [Doi] => 10.37349/ent.2021.00001 [Published] => August 05, 2021 [Viewed] => 1837 [Downloaded] => 33 [Subject] => Editorial [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00001 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:1–6 [Recommend] => 0 [Keywords] => [DetailTitle] => [DetailUrl] => [Id] => 10041 [ris] => https://www.explorationpub.com/uploads/Article/A10041/8cfeddfc154bfd4bf42927e3a747b941.ris [bib] => https://www.explorationpub.com/uploads/Article/A10041/eb80cdbee35b3abb781b2320d1dca92f.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-05-27 [CitethisArticle] => Franco R. Science plus technology to address challenges in determining the efficacy of neuroprotective/neurorestorative therapies. Explor Neuroprot Ther. 2021;1:1-6. https://doi.org/10.37349/ent.2021.00001 [Jindex] => 0 [CEmail] => rfranco@ub.edu, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => Science plus technology to address challenges in determining the efficacy of neuroprotective/neurorestorative therapies,,,Rafael Franco [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Rafael Franco ) [1] => Array ( [ArticleId] => 122 [Create_Time] => 2021-04-20 [zipUrl] => https://www.explorationpub.com/uploads/zip/202108/20210826040057.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10042/10042.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10042/10042.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10042/10042_cover.png [JournalsId] => 7 [Title] => P2X7 receptor involvement in COVID-19 disease [Abstract] => [AbstractComplete] => [Names] => Peter Illes [CName] => PeterIlles, [Doi] => 10.37349/ent.2021.00002 [Published] => August 05, 2021 [Viewed] => 1258 [Downloaded] => 39 [Subject] => Letter to the Editor [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00002 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:7–9 [Recommend] => 0 [Keywords] => COVID-19, SARS-CoV-2, P2X7 receptor, angiotensin-converting enzyme 2, cytokine storm, central nervous system complications [DetailTitle] => [DetailUrl] => [Id] => 10042 [ris] => https://www.explorationpub.com/uploads/Article/A10042/798eecc0cf93fa8bb06db49d646685f5.ris [bib] => https://www.explorationpub.com/uploads/Article/A10042/a0416a81ddd33ec3ab8b37bba463ad9d.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Illes P. P2X7 receptor involvement in COVID-19 disease. Explor Neuroprot Ther. 2021;1:7-9. https://doi.org/10.37349/ent.2021.00002 [Jindex] => 0 [CEmail] => peter.illes@medizin.uni-leipzig.de, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => P2X7 receptor involvement in COVID-19 disease, COVID-19, SARS-CoV-2, P2X7 receptor, angiotensin-converting enzyme 2, cytokine storm, central nervous system complications,,Peter Illes [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Peter Illes ) [2] => Array ( [ArticleId] => 139 [Create_Time] => 2021-06-21 [zipUrl] => https://www.explorationpub.com/uploads/zip/202211/20221108022101.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10043/10043.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10043/10043.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10043/10043_cover.png [JournalsId] => 7 [Title] => Cholesterol in autism spectrum disorders [Abstract] => The autism spectrum disorder (ASD) comprises a series of neurological diseases that share serious alterations of the development of the central nervous system. The degree of disability may vary so t [AbstractComplete] =>

The autism spectrum disorder (ASD) comprises a series of neurological diseases that share serious alterations of the development of the central nervous system. The degree of disability may vary so that Asperger’s may have a relatively normal life and get positions of responsibility in corporations and even in Governments, whereas other ASD sufferers are fully dependent on caregivers and have serious cognitive deficits. Although the first cases of autism were detected by looking at failures in metabolism, e.g., phenylketonuria, to later identify the faulty gene, today the trend is the opposite, first obtaining the exome and minimizing the look for altered parameters in blood, urine, etc. Cholesterol is key for neural development as it is not able to cross the blood brain barrier. Therefore, any gene or environmental factor that affects cholesterol synthesis will impact early developmental stages eventually leading to a disease within the autism spectrum and/or schizophrenia. This review provides data of the relevance of cholesterol dyshomeostasis in autism spectrum disorders. Determining biochemical parameters in body fluids should help to provide new therapeutic approaches in some cases of autism.

[Names] => Rafael Franco ... Irene Reyes-Resina [CName] => RafaelFranco, [Doi] => 10.37349/ent.2021.00003 [Published] => August 05, 2021 [Viewed] => 3583 [Downloaded] => 100 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00003 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 44 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:10–18 [Recommend] => 0 [Keywords] => Autism spectrum disorder, Asperger syndrome, cholesterol, cholesterol dyshomeostasis, Rett syndrome, Smith-Lemli-Opitz syndrome, blood brain barrier [DetailTitle] => Cholesterol Dyshomeostasis in Neurological Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/44 [Id] => 10043 [ris] => https://www.explorationpub.com/uploads/Article/A10043/861de3b74958867404156c4815ec1144.ris [bib] => https://www.explorationpub.com/uploads/Article/A10043/f810521c29a79d832493e5191074f0d9.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Franco R, Rivas-Santisteban R, Navarro G, Reyes-Resina I. Cholesterol in autism spectrum disorders. Explor Neuroprot Ther. 2021;1:10-8. https://doi.org/10.37349/ent.2021.00003 [Jindex] => 0 [CEmail] => rfranco@ub.edu, [Ris_Time] => 0000-00-00 00:00:00 [Bib_Time] => 0000-00-00 00:00:00 [KeysWordContens] => Cholesterol in autism spectrum disorders, Autism spectrum disorder, Asperger syndrome, cholesterol, cholesterol dyshomeostasis, Rett syndrome, Smith-Lemli-Opitz syndrome, blood brain barrier, The autism spectrum disorder (ASD) comprises a series of neurological diseases that share serious alterations of the development of the central nervous system. The degree of disability may vary so that Asperger’s may have a relatively normal life and get positions of responsibility in corporations and even in Governments, whereas other ASD sufferers are fully dependent on caregivers and have serious cognitive deficits. Although the first cases of autism were detected by looking at failures in metabolism, e.g., phenylketonuria, to later identify the faulty gene, today the trend is the opposite, first obtaining the exome and minimizing the look for altered parameters in blood, urine, etc. Cholesterol is key for neural development as it is not able to cross the blood brain barrier. Therefore, any gene or environmental factor that affects cholesterol synthesis will impact early developmental stages eventually leading to a disease within the autism spectrum and/or schizophrenia. This review provides data of the relevance of cholesterol dyshomeostasis in autism spectrum disorders. Determining biochemical parameters in body fluids should help to provide new therapeutic approaches in some cases of autism. ,Rafael Franco ... Irene Reyes-Resina [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Rafael Franco, Rafael Rivas-Santisteban, Gemma Navarro, Irene Reyes-Resina ) [3] => Array ( [ArticleId] => 141 [Create_Time] => 2021-06-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230804023425.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10044/10044.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10044/10044.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10044/10044_cover.png [JournalsId] => 7 [Title] => Neurological complications during HIV infection [Abstract] => Early in the course of infection, human immunodeficiency virus (HIV) is able to enter the central nervous system where it stablishes a permanent reservoir. Current antiretroviral therapies do not ef [AbstractComplete] =>

Early in the course of infection, human immunodeficiency virus (HIV) is able to enter the central nervous system where it stablishes a permanent reservoir. Current antiretroviral therapies do not efficiently cross the blood-brain barrier and therefore do not reach the HIV located in the central nervous system. Consequently, HIV infection can often be associated with neurocognitive impairment and HIV-associated dementia. The purpose of this review is to brief the reader into the world of neurological complications arising from HIV infection. Mechanisms by which HIV directly or indirectly impairs the central nervous system are discussed, as well as other factors influencing or contributing to the impairment, and the animal models currently used to perform research on the topic.

[Names] => Jose M. Martinez-Navio [CName] => Jose M.Martinez-Navio, [Doi] => 10.37349/ent.2021.00004 [Published] => August 05, 2021 [Viewed] => 4232 [Downloaded] => 220 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00004 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:19–32 [Recommend] => 0 [Keywords] => HIV, neurological complications, HIV-associated neurocognitive disorders, dementia, inflammation [DetailTitle] => [DetailUrl] => [Id] => 10044 [ris] => https://www.explorationpub.com/uploads/Article/A10044/043d3be58b8214d0b8f70afc90b3d65b.ris [bib] => https://www.explorationpub.com/uploads/Article/A10044/6e592088f3074770208588f480306fdf.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-05-27 [CitethisArticle] => Martinez-Navio JM. Neurological complications during HIV infection. Explor Neuroprot Ther. 2021;1:19-32. https://doi.org/10.37349/ent.2021.00004 [Jindex] => 0 [CEmail] => martinez-navio@med.miami.edu, [Ris_Time] => 2023-08-04 02:34:25 [Bib_Time] => 2023-08-04 02:34:25 [KeysWordContens] => Neurological complications during HIV infection, HIV, neurological complications, HIV-associated neurocognitive disorders, dementia, inflammation, Early in the course of infection, human immunodeficiency virus (HIV) is able to enter the central nervous system where it stablishes a permanent reservoir. Current antiretroviral therapies do not efficiently cross the blood-brain barrier and therefore do not reach the HIV located in the central nervous system. Consequently, HIV infection can often be associated with neurocognitive impairment and HIV-associated dementia. The purpose of this review is to brief the reader into the world of neurological complications arising from HIV infection. Mechanisms by which HIV directly or indirectly impairs the central nervous system are discussed, as well as other factors influencing or contributing to the impairment, and the animal models currently used to perform research on the topic. ,Jose M. Martinez-Navio [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Jose M. Martinez-Navio ) [4] => Array ( [ArticleId] => 156 [Create_Time] => 2021-07-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230804024451.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10045/10045.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10045/10045.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10045/10045_cover.png [JournalsId] => 7 [Title] => Gut microbial imbalance and neurodegenerative proteinopathies: from molecular mechanisms to prospects of clinical applications [Abstract] => The pathogenic basis behind some of the most prevalent neurodegenerative diseases in advanced societies, known as proteinopathies, deals with alterations in protein homeostasis. Despite the broad di [AbstractComplete] =>

The pathogenic basis behind some of the most prevalent neurodegenerative diseases in advanced societies, known as proteinopathies, deals with alterations in protein homeostasis. Despite the broad diversity of clinical symptoms, they share a remarkably common feature that is the serious neuronal loss in several disease-specific brain regions due to the presence of toxic aggregations of misfolded proteins. So far, research efforts have been insufficient to decipher the exact molecular mechanisms that trigger the conformational change from a functional healthy protein to its pathological version. This is a sine qua non condition to progress in developing new approaches and treatments for these diseases for which there is no cure. Currently, it is well accepted that perturbations in gut microbiota composition negatively impact a wide range of brain processes via the gut-brain axis which increases host susceptibility to neurodegenerative disorders. In this context, modulate the microbial ecosystem colonizing the gastrointestinal tract may be a promising therapeutic approach in the management of proteinopathies. This review aims to provide an updated view of the role that gut microbiota poses in the pathogenesis of Parkinson’s disease, Alzheimer’s disease and Huntington’s disease, the most common neurodegenerative proteinopathies, and of the possibility of translating this knowledge into effective and safe clinical microbiota-based interventions, especially those designed to afford neuroprotection.

[Names] => Paula Alonso-García ... Eva Martínez-Pinilla [CName] => RebecaMartín, [Doi] => 10.37349/ent.2021.00005 [Published] => August 05, 2021 [Viewed] => 2427 [Downloaded] => 92 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00005 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:33–54 [Recommend] => 0 [Keywords] => Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, gut microbiota, protein aggregation, dysbiosis, gut-brain axis, probiotics, life biotherapeutics [DetailTitle] => [DetailUrl] => [Id] => 10045 [ris] => https://www.explorationpub.com/uploads/Article/A10045/c10310841c907ab6f40e6d08f53b7402.ris [bib] => https://www.explorationpub.com/uploads/Article/A10045/3ac97b5b3b70aa22e1244d25d5226ba1.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Alonso-García P, Martín R, Martínez-Pinilla E. Gut microbial imbalance and neurodegenerative proteinopathies: from molecular mechanisms to prospects of clinical applications. Explor Neuroprot Ther. 2021;1:33-54. https://doi.org/10.37349/ent.2021.00005 [Jindex] => 0 [CEmail] => rebeca.martin-rosique@inrae.fr, [Ris_Time] => 2023-08-04 02:44:51 [Bib_Time] => 2023-08-04 02:44:51 [KeysWordContens] => Gut microbial imbalance and neurodegenerative proteinopathies: from molecular mechanisms to prospects of clinical applications, Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, gut microbiota, protein aggregation, dysbiosis, gut-brain axis, probiotics, life biotherapeutics, The pathogenic basis behind some of the most prevalent neurodegenerative diseases in advanced societies, known as proteinopathies, deals with alterations in protein homeostasis. Despite the broad diversity of clinical symptoms, they share a remarkably common feature that is the serious neuronal loss in several disease-specific brain regions due to the presence of toxic aggregations of misfolded proteins. So far, research efforts have been insufficient to decipher the exact molecular mechanisms that trigger the conformational change from a functional healthy protein to its pathological version. This is a sine qua non condition to progress in developing new approaches and treatments for these diseases for which there is no cure. Currently, it is well accepted that perturbations in gut microbiota composition negatively impact a wide range of brain processes via the gut-brain axis which increases host susceptibility to neurodegenerative disorders. In this context, modulate the microbial ecosystem colonizing the gastrointestinal tract may be a promising therapeutic approach in the management of proteinopathies. This review aims to provide an updated view of the role that gut microbiota poses in the pathogenesis of Parkinson’s disease, Alzheimer’s disease and Huntington’s disease, the most common neurodegenerative proteinopathies, and of the possibility of translating this knowledge into effective and safe clinical microbiota-based interventions, especially those designed to afford neuroprotection. ,Paula Alonso-García ... Eva Martínez-Pinilla [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Paula Alonso-García, Rebeca Martín, Eva Martínez-Pinilla ) [5] => Array ( [ArticleId] => 157 [Create_Time] => 2021-08-03 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230804025203.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10046/10046.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10046/10046.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10046/10046_cover.png [JournalsId] => 7 [Title] => Therapeutic potential of the cannabinoid receptor 2 in neuropsychiatry [Abstract] => Since the identification and cloning of the cannabinoid receptor 2 (CB2R), several studies focused on the characterization of its physiological and pathological role. Initially, CB2R was considered [AbstractComplete] =>

Since the identification and cloning of the cannabinoid receptor 2 (CB2R), several studies focused on the characterization of its physiological and pathological role. Initially, CB2R was considered as the peripheral cannabinoid receptor due to its detection in the rat spleen and leukocyte subpopulation in humans. Later, CB2R was identified in different brain regions significantly modifying the landscape and pointing out its role in a wide variety of central physiological functions and pathological conditions. Additional research also detected the expression of CB2R in neurons, microglia, and astroglia in different brain regions. Indeed, the findings collected to date support a significant function of CB2R in anxiety, depression, schizophrenia, and additional neuropsychiatric disorders. This review gathers the most relevant literature regarding new advances about the role of CB2R in a variety of neuropsychiatric conditions, with special emphasis on its potential as a new therapeutic target for the treatment of different psychiatric disorders.

[Names] => María S. García-Gutiérrez ... Jorge Manzanares [CName] => JorgeManzanares, [Doi] => 10.37349/ent.2021.00006 [Published] => August 05, 2021 [Viewed] => 4214 [Downloaded] => 211 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00006 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:55–71 [Recommend] => 0 [Keywords] => Cannabinoid receptor 2, psychiatry, emotional response, anxiety, depression, schizophrenia, bipolar disorder [DetailTitle] => [DetailUrl] => [Id] => 10046 [ris] => https://www.explorationpub.com/uploads/Article/A10046/4022bd16f01f3b14405c7bcf75c566a6.ris [bib] => https://www.explorationpub.com/uploads/Article/A10046/99216c199227a2bd32dd0aae99cb7410.bib [ens] => [Cited] => 3 [Cited_Time] => 2024-05-27 [CitethisArticle] => García-Gutiérrez MS, Navarrete F, Gasparyan A, Manzanares J. Therapeutic potential of the cannabinoid receptor 2 in neuropsychiatry. Explor Neuroprot Ther. 2021;1:55-71. https://doi.org/10.37349/ent.2021.00006 [Jindex] => 0 [CEmail] => jmanzanares@goumh.umh.es, [Ris_Time] => 2023-08-04 02:52:03 [Bib_Time] => 2023-08-04 02:52:03 [KeysWordContens] => Therapeutic potential of the cannabinoid receptor 2 in neuropsychiatry, Cannabinoid receptor 2, psychiatry, emotional response, anxiety, depression, schizophrenia, bipolar disorder, Since the identification and cloning of the cannabinoid receptor 2 (CB2R), several studies focused on the characterization of its physiological and pathological role. Initially, CB2R was considered as the peripheral cannabinoid receptor due to its detection in the rat spleen and leukocyte subpopulation in humans. Later, CB2R was identified in different brain regions significantly modifying the landscape and pointing out its role in a wide variety of central physiological functions and pathological conditions. Additional research also detected the expression of CB2R in neurons, microglia, and astroglia in different brain regions. Indeed, the findings collected to date support a significant function of CB2R in anxiety, depression, schizophrenia, and additional neuropsychiatric disorders. This review gathers the most relevant literature regarding new advances about the role of CB2R in a variety of neuropsychiatric conditions, with special emphasis on its potential as a new therapeutic target for the treatment of different psychiatric disorders. ,María S. García-Gutiérrez ... Jorge Manzanares [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => María S. García-Gutiérrez, Francisco Navarrete, Ani Gasparyan, Jorge Manzanares ) [6] => Array ( [ArticleId] => 182 [Create_Time] => 2021-10-03 [zipUrl] => https://www.explorationpub.com/uploads/zip/202111/20211102034601.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10047/10047.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10047/10047.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10047/10047_cover.png [JournalsId] => 7 [Title] => T-cell based immunotherapies for Parkinson’s disease [Abstract] => Current evidence indicates that neurodegeneration of dopaminergic neurons of the substantia nigra associated to Parkinson’s disease is a consequence of a neuroinflammatory process in whic [AbstractComplete] =>

Current evidence indicates that neurodegeneration of dopaminergic neurons of the substantia nigra associated to Parkinson’s disease is a consequence of a neuroinflammatory process in which microglial cells play a central role. The initial activation of microglial cells is triggered by pathogenic protein inclusions, which are mainly composed by α-synuclein. Importantly, these pathogenic forms of α-synuclein subsequently induce a T-cell-mediated autoimmune response to dopaminergic neurons. Depending on their functional phenotype, these autoreactive T-cells might shape the functional features of activated microglia. T-cells bearing pro-inflammatory phenotypes such as T-helper (Th)1 or Th17 promote a chronic inflammatory behaviour on microglia, whilst anti-inflammatory T-cells, such as regulatory T-cells (Treg) favour the acquisition of neuroprotective features by microglia. Thus, T-cells play a fundamental role in the development of neuroinflammation and neurodegeneration involved in Parkinson’s disease. This review summarizes the evidence indicating that not only CD4+ T-cells, but also CD8+ T-cells play an important role in the physiopathology of Parkinson’s disease. Next, this review analyses the different T-cell epitopes derived from the pathogenic forms of α-synuclein involved in the autoimmune response associated to Parkinson’s disease in animal models and humans. It also summarizes the requirement of specific alleles of major histocompatibility complexes (MHC) class I and class II necessaries for the presentation of CD8+ and CD4+ T-cell epitopes from the pathogenic forms of α-synuclein in both humans and animal models. Finally, this work summarizes and discusses a number of experimental immunotherapies that aim to strengthen the Treg response or to dampen the inflammatory T-cell response as a therapeutic approach in animal models of Parkinson’s disease.

[Names] => Rodrigo Pacheco [CName] => RodrigoPacheco, [Doi] => 10.37349/ent.2021.00007 [Published] => October 29, 2021 [Viewed] => 2526 [Downloaded] => 115 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00007 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:72–85 [Recommend] => 0 [Keywords] => Parkinson’s disease, neuroinflammation, neurodegeneration, T cells, regulatory T cells, alpha-synuclein, immunotherapy [DetailTitle] => [DetailUrl] => [Id] => 10047 [ris] => https://www.explorationpub.com/uploads/Article/A10047/6e281e6c58b74e9f800d1274f98b1df7.ris [bib] => https://www.explorationpub.com/uploads/Article/A10047/c0b5605de9fdd8c5804764f760b4a4ea.bib [ens] => [Cited] => 4 [Cited_Time] => 2024-05-27 [CitethisArticle] => Pacheco R. T-cell based immunotherapies for Parkinson’s disease. Explor Neuroprot Ther. 2021;1:72-85. https://doi.org/10.37349/ent.2021.00007 [Jindex] => 1 [CEmail] => rpacheco@cienciavida.org, [Ris_Time] => 2021-11-02 03:46:01 [Bib_Time] => 2021-11-02 03:46:01 [KeysWordContens] => T-cell based immunotherapies for Parkinson’s disease, Parkinson’s disease, neuroinflammation, neurodegeneration, T cells, regulatory T cells, alpha-synuclein, immunotherapy, Current evidence indicates that neurodegeneration of dopaminergic neurons of the substantia nigra associated to Parkinson’s disease is a consequence of a neuroinflammatory process in which microglial cells play a central role. The initial activation of microglial cells is triggered by pathogenic protein inclusions, which are mainly composed by α-synuclein. Importantly, these pathogenic forms of α-synuclein subsequently induce a T-cell-mediated autoimmune response to dopaminergic neurons. Depending on their functional phenotype, these autoreactive T-cells might shape the functional features of activated microglia. T-cells bearing pro-inflammatory phenotypes such as T-helper (Th)1 or Th17 promote a chronic inflammatory behaviour on microglia, whilst anti-inflammatory T-cells, such as regulatory T-cells (Treg) favour the acquisition of neuroprotective features by microglia. Thus, T-cells play a fundamental role in the development of neuroinflammation and neurodegeneration involved in Parkinson’s disease. This review summarizes the evidence indicating that not only CD4+ T-cells, but also CD8+ T-cells play an important role in the physiopathology of Parkinson’s disease. Next, this review analyses the different T-cell epitopes derived from the pathogenic forms of α-synuclein involved in the autoimmune response associated to Parkinson’s disease in animal models and humans. It also summarizes the requirement of specific alleles of major histocompatibility complexes (MHC) class I and class II necessaries for the presentation of CD8+ and CD4+ T-cell epitopes from the pathogenic forms of α-synuclein in both humans and animal models. Finally, this work summarizes and discusses a number of experimental immunotherapies that aim to strengthen the Treg response or to dampen the inflammatory T-cell response as a therapeutic approach in animal models of Parkinson’s disease. ,Rodrigo Pacheco [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Rodrigo Pacheco ) [7] => Array ( [ArticleId] => 183 [Create_Time] => 2021-10-12 [zipUrl] => https://www.explorationpub.com/uploads/zip/202201/20220107035155.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10049/10049.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10049/10049.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10049/10049_cover.png [JournalsId] => 7 [Title] => Immunization with neural-derived peptides as a neuroprotective therapy for spinal cord injury [Abstract] => Spinal cord injury (SCI) induces several destructive events that develop immediately after the primary insult. These phenomena increase tissue damage; that is why, numerous therapeutic approaches ar [AbstractComplete] =>

Spinal cord injury (SCI) induces several destructive events that develop immediately after the primary insult. These phenomena increase tissue damage; that is why, numerous therapeutic approaches are studied in order to neutralize these destructive mechanisms. In line with this, several studies indicate that after injury, neural tissue could be protected by an adaptive immune response directed against self-antigens. Immunization with neural-derived peptides (INDP) reduces secondary degeneration of neurons after spinal cord insult and promotes a significant motor recovery. The combination of antioxidants or other immunomodulatory peptides after SCI can improve the protective effect induced by INDP. INDP in acute SCI is a promising strategy, so further studies should be addressed to be able to formulate the best strategy.

[Names] => Andrea Paola Ibarra-García, Antonio Ibarra [CName] => AntonioIbarra, [Doi] => 10.37349/ent.2021.00009 [Published] => October 29, 2021 [Viewed] => 1507 [Downloaded] => 49 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00009 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:111–120 [Recommend] => 0 [Keywords] => A91, immunization, paraplegia, protective autoimmunity [DetailTitle] => [DetailUrl] => [Id] => 10049 [ris] => https://www.explorationpub.com/uploads/Article/A10049/25969b74c9bd34731e4cd111bb94ed91.ris [bib] => https://www.explorationpub.com/uploads/Article/A10049/4d55c0922630b404c24767e75bbf84bf.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Ibarra-García AP, Ibarra A. Immunization with neural-derived peptides as a neuroprotective therapy for spinal cord injury. Explor Neuroprot Ther. 2021;1:111-20. https://doi.org/10.37349/ent.2021.00009 [Jindex] => 1 [CEmail] => jose.ibarra@anahuac.mx, [Ris_Time] => 2021-11-02 03:56:49 [Bib_Time] => 2021-11-02 03:56:49 [KeysWordContens] => Immunization with neural-derived peptides as a neuroprotective therapy for spinal cord injury, A91, immunization, paraplegia, protective autoimmunity, Spinal cord injury (SCI) induces several destructive events that develop immediately after the primary insult. These phenomena increase tissue damage; that is why, numerous therapeutic approaches are studied in order to neutralize these destructive mechanisms. In line with this, several studies indicate that after injury, neural tissue could be protected by an adaptive immune response directed against self-antigens. Immunization with neural-derived peptides (INDP) reduces secondary degeneration of neurons after spinal cord insult and promotes a significant motor recovery. The combination of antioxidants or other immunomodulatory peptides after SCI can improve the protective effect induced by INDP. INDP in acute SCI is a promising strategy, so further studies should be addressed to be able to formulate the best strategy. ,Andrea Paola Ibarra-García, Antonio Ibarra [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Andrea Paola Ibarra-García, Antonio Ibarra ) [8] => Array ( [ArticleId] => 184 [Create_Time] => 2021-10-09 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230804030127.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10048/10048.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10048/10048.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10048/10048_cover.png [JournalsId] => 7 [Title] => Striking a balance: PIP2 and PIP3 signaling in neuronal health and disease [Abstract] => Phosphoinositides are membrane phospholipids involved in a variety of cellular processes like growth, development, metabolism, and transport. This review focuses on the maintenance of cellular homeo [AbstractComplete] =>

Phosphoinositides are membrane phospholipids involved in a variety of cellular processes like growth, development, metabolism, and transport. This review focuses on the maintenance of cellular homeostasis of phosphatidylinositol 4,5-bisphosphate (PIP2), and phosphatidylinositol 3,4,5-trisphosphate (PIP3). The critical balance of these PIPs is crucial for regulation of neuronal form and function. The activity of PIP2 and PIP3 can be regulated through kinases, phosphatases, phospholipases and cholesterol microdomains. PIP2 and PIP3 carry out their functions either indirectly through their effectors activating integral signaling pathways, or through direct regulation of membrane channels, transporters, and cytoskeletal proteins. Any perturbations to the balance between PIP2 and PIP3 signaling result in neurodevelopmental and neurodegenerative disorders. This review will discuss the upstream modulators and downstream effectors of the PIP2 and PIP3 signaling, in the context of neuronal health and disease.

[Names] => Kamran Tariq, Bryan W. Luikart [CName] => Bryan W.Luikart, [Doi] => 10.37349/ent.2021.00008 [Published] => October 29, 2021 [Viewed] => 6237 [Downloaded] => 282 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00008 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 44 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:86–110 [Recommend] => 0 [Keywords] => Phosphoinositides, cholesterol, autism, Alzheimer’s, ion channels, cytoskeleton, AKT, mammalian target of rapamycin [DetailTitle] => Cholesterol Dyshomeostasis in Neurological Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/44 [Id] => 10048 [ris] => https://www.explorationpub.com/uploads/Article/A10048/fdae09dac1078d26219bdc7f19d3d1ec.ris [bib] => https://www.explorationpub.com/uploads/Article/A10048/ae879ce19a4b290a54c5520b860e35e1.bib [ens] => [Cited] => 16 [Cited_Time] => 2024-05-27 [CitethisArticle] => Tariq K, Luikart BW. Striking a balance: PIP2 and PIP3 signaling in neuronal health and disease. Explor Neuroprot Ther. 2021;1:86-110. https://doi.org/10.37349/ent.2021.00008 [Jindex] => 1 [CEmail] => Bryan.W.Luikart@Dartmouth.edu, [Ris_Time] => 2023-08-04 03:01:27 [Bib_Time] => 2023-08-04 03:01:27 [KeysWordContens] => Striking a balance: PIP2 and PIP3 signaling in neuronal health and disease, Phosphoinositides, cholesterol, autism, Alzheimer’s, ion channels, cytoskeleton, AKT, mammalian target of rapamycin, Phosphoinositides are membrane phospholipids involved in a variety of cellular processes like growth, development, metabolism, and transport. This review focuses on the maintenance of cellular homeostasis of phosphatidylinositol 4,5-bisphosphate (PIP2), and phosphatidylinositol 3,4,5-trisphosphate (PIP3). The critical balance of these PIPs is crucial for regulation of neuronal form and function. The activity of PIP2 and PIP3 can be regulated through kinases, phosphatases, phospholipases and cholesterol microdomains. PIP2 and PIP3 carry out their functions either indirectly through their effectors activating integral signaling pathways, or through direct regulation of membrane channels, transporters, and cytoskeletal proteins. Any perturbations to the balance between PIP2 and PIP3 signaling result in neurodevelopmental and neurodegenerative disorders. This review will discuss the upstream modulators and downstream effectors of the PIP2 and PIP3 signaling, in the context of neuronal health and disease. ,Kamran Tariq, Bryan W. Luikart [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Kamran Tariq, Bryan W. Luikart ) [9] => Array ( [ArticleId] => 198 [Create_Time] => 2021-10-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202111/20211101051428.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100410/100410.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100410/100410.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100410/100410_cover.png [JournalsId] => 7 [Title] => Maternal imprinting, mitochondrial DNA, nuclear DNA and Alzheimer’s disease [Abstract] => Familial early-onset Alzheimer’s disease (AD) is more probable in individuals coming from mothers diagnosed with AD than from fathers diagnosed with AD. Studies in animal models have show [AbstractComplete] =>

Familial early-onset Alzheimer’s disease (AD) is more probable in individuals coming from mothers diagnosed with AD than from fathers diagnosed with AD. Studies in animal models have shown maternal imprinting due to the transmission to the embryo of altered material in the ovum. In the case of transgenic animals harboring a mutated form of the human amyloid precursor protein (APP), offspring from crosses with wild-type (WT) fathers and transgenic mothers display more abnormalities than offspring from crosses with transgenic fathers and WT mothers. Expression of the mutated APP in the ovum may lead to alterations that may be genetic and/or epigenetic in the nuclear and/or the mitochondrial DNA. These modifications that are transmitted to the new living beings affect more mitochondrial proteins and, therefore, the mitochondrial function may be affected in adulthood by trends present in the ovum.

[Names] => Alberto Pérez-Mediavilla, Marta Zamarbide [CName] => MartaZamarbide, [Doi] => 10.37349/ent.2021.00010 [Published] => October 29, 2021 [Viewed] => 1194 [Downloaded] => 35 [Subject] => Perspective [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00010 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:121–126 [Recommend] => 0 [Keywords] => β-amyloid, protein aggregates, synuclein, fibrillary tangles, mitochondria, ovum, mitophagy [DetailTitle] => [DetailUrl] => [Id] => 100410 [ris] => https://www.explorationpub.com/uploads/Article/A100410/56037bfe464a02f875bad1d3341b967e.ris [bib] => https://www.explorationpub.com/uploads/Article/A100410/438bb7fbf4710577c63a31796b48be30.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Pérez-Mediavilla A, Zamarbide M. Maternal imprinting, mitochondrial DNA, nuclear DNA and Alzheimer’s disease. Explor Neuroprot Ther. 2021;1:121-6. https://doi.org/10.37349/ent.2021.00010 [Jindex] => 1 [CEmail] => mzamarbide@unav.es, [Ris_Time] => 2021-10-29 06:09:37 [Bib_Time] => 2021-10-29 08:30:04 [KeysWordContens] => Maternal imprinting, mitochondrial DNA, nuclear DNA and Alzheimer’s disease, β-amyloid, protein aggregates, synuclein, fibrillary tangles, mitochondria, ovum, mitophagy, Familial early-onset Alzheimer’s disease (AD) is more probable in individuals coming from mothers diagnosed with AD than from fathers diagnosed with AD. Studies in animal models have shown maternal imprinting due to the transmission to the embryo of altered material in the ovum. In the case of transgenic animals harboring a mutated form of the human amyloid precursor protein (APP), offspring from crosses with wild-type (WT) fathers and transgenic mothers display more abnormalities than offspring from crosses with transgenic fathers and WT mothers. Expression of the mutated APP in the ovum may lead to alterations that may be genetic and/or epigenetic in the nuclear and/or the mitochondrial DNA. These modifications that are transmitted to the new living beings affect more mitochondrial proteins and, therefore, the mitochondrial function may be affected in adulthood by trends present in the ovum. ,Alberto Pérez-Mediavilla, Marta Zamarbide [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Alberto Pérez-Mediavilla, Marta Zamarbide ) [10] => Array ( [ArticleId] => 210 [Create_Time] => 2021-12-07 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230804030707.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100411/100411.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100411/100411.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100411/100411_cover.png [JournalsId] => 7 [Title] => Peroxisomes in intracellular cholesterol transport: from basic physiology to brain pathology [Abstract] => Peroxisomes are actively involved in the metabolism of various lipids including fatty acids, ether phospholipids, bile acids as well as the processing of reactive oxygen and nitrogen species. Recent [AbstractComplete] =>

Peroxisomes are actively involved in the metabolism of various lipids including fatty acids, ether phospholipids, bile acids as well as the processing of reactive oxygen and nitrogen species. Recent studies show that peroxisomes can regulate cholesterol homeostasis by mediating cholesterol transport from the lysosomes to the endoplasmic reticulum and towards primary cilium as well. Disruptions of peroxisome biogenesis or functions lead to peroxisomal disorders that usually involve neurological deficits. Peroxisomal dysfunction is also linked to several neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. In many peroxisomal disorders and neurodegenerative diseases, aberrant cholesterol accumulation is frequently encountered yet largely neglected. This review discusses the current understanding of the mechanisms by which peroxisomes facilitate cholesterol trafficking within the cell and the pathological conditions related to impaired cholesterol transport by peroxisomes, with the hope to inspire future development of the treatments for peroxisomal disorders and neurodegenerative diseases.

[Names] => Jian Xiao ... Jie Luo [CName] => JieLuo, [Doi] => 10.37349/ent.2021.00011 [Published] => December 30, 2021 [Viewed] => 3008 [Downloaded] => 130 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00011 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 44 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:127–145 [Recommend] => 0 [Keywords] => Peroxisome, cholesterol transport, nervous system, peroxisomal disorders [DetailTitle] => Cholesterol Dyshomeostasis in Neurological Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/44 [Id] => 100411 [ris] => https://www.explorationpub.com/uploads/Article/A100411/8c8ae2f6186f193b9faac0b80f726ed7.ris [bib] => https://www.explorationpub.com/uploads/Article/A100411/bb5d2c2146bc33e6063369919871fca0.bib [ens] => [Cited] => 3 [Cited_Time] => 2024-05-27 [CitethisArticle] => Xiao J, Song BL, Luo J. Peroxisomes in intracellular cholesterol transport: from basic physiology to brain pathology. Explor Neuroprot Ther. 2021;1:127-45. https://doi.org/10.37349/ent.2021.00011 [Jindex] => 1 [CEmail] => jieluo@whu.edu.cn, [Ris_Time] => 2023-08-04 03:07:07 [Bib_Time] => 2023-08-04 03:07:07 [KeysWordContens] => Peroxisomes in intracellular cholesterol transport: from basic physiology to brain pathology, Peroxisome, cholesterol transport, nervous system, peroxisomal disorders, Peroxisomes are actively involved in the metabolism of various lipids including fatty acids, ether phospholipids, bile acids as well as the processing of reactive oxygen and nitrogen species. Recent studies show that peroxisomes can regulate cholesterol homeostasis by mediating cholesterol transport from the lysosomes to the endoplasmic reticulum and towards primary cilium as well. Disruptions of peroxisome biogenesis or functions lead to peroxisomal disorders that usually involve neurological deficits. Peroxisomal dysfunction is also linked to several neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. In many peroxisomal disorders and neurodegenerative diseases, aberrant cholesterol accumulation is frequently encountered yet largely neglected. This review discusses the current understanding of the mechanisms by which peroxisomes facilitate cholesterol trafficking within the cell and the pathological conditions related to impaired cholesterol transport by peroxisomes, with the hope to inspire future development of the treatments for peroxisomal disorders and neurodegenerative diseases. ,Jian Xiao ... Jie Luo [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Jian Xiao, Bao-Liang Song, Jie Luo ) [11] => Array ( [ArticleId] => 214 [Create_Time] => 2021-12-09 [zipUrl] => https://www.explorationpub.com/uploads/zip/202112/20211230073707.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100412/100412.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100412/100412.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100412/100412_cover.png [JournalsId] => 7 [Title] => Advancing diagnosis and treatment of Niemann-Pick C disease through biomarker discovery [Abstract] => Niemann-Pick C disease is a rare neurodegenerative, lysosomal storage disease caused by accumulation of unesterified cholesterol. Diagnosis of the disease is often delayed due to its rarity, the het [AbstractComplete] =>

Niemann-Pick C disease is a rare neurodegenerative, lysosomal storage disease caused by accumulation of unesterified cholesterol. Diagnosis of the disease is often delayed due to its rarity, the heterogeneous presentation, and the early non-specific symptoms. The discovery of disease-specific biomarkers—cholestane-3β,5α,6β-triol (C-triol), trihydroxycholanic acid glycinate (TCG) and N-palmitoyl-O-phosphocholineserine [PPCS, initially referred to as lysosphingomyelin-509 (lysoSM-509)]—has led to development of non-invasive, blood-based diagnostics. Dissemination of these rapid, sensitive, and specific clinical assays has accelerated diagnosis. Moreover, the superior receiver operating characteristic of the TCG bile acid biomarker and its detection in dried blood spots has also facilitated development of a newborn screen for NPC, which is currently being piloted in New York state. The C-triol, TCG and PPCS biomarkers have also been proved useful for monitoring treatment response in peripheral tissues, but are uninformative with respect to treatment efficacy in the central nervous system (CNS). A major gap for the field is the lack of a validated, non-invasive biomarker to monitor the course of disease and CNS response to therapy.

[Names] => Xuntian Jiang, Daniel S. Ory [CName] => Daniel S.Ory, [Doi] => 10.37349/ent.2021.00012 [Published] => December 30, 2021 [Viewed] => 2113 [Downloaded] => 88 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00012 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 44 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:146–158 [Recommend] => 0 [Keywords] => Niemann-Pick C, cholesterol, biomarkers, diagnosis, oxysterol, bile acids [DetailTitle] => Cholesterol Dyshomeostasis in Neurological Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/44 [Id] => 100412 [ris] => https://www.explorationpub.com/uploads/Article/A100412/65a3d4d2fec2a190961d59ae122ecf18.ris [bib] => https://www.explorationpub.com/uploads/Article/A100412/ac77a1670de43c4c1d2724a9ce1efd22.bib [ens] => [Cited] => 10 [Cited_Time] => 2024-05-27 [CitethisArticle] => Jiang X, Ory DS. Advancing diagnosis and treatment of Niemann-Pick C disease through biomarker discovery. Explor Neuroprot Ther. 2021;1:146-58. https://doi.org/10.37349/ent.2021.00012 [Jindex] => 0 [CEmail] => dory@casmatx.com, [Ris_Time] => 2021-12-30 07:37:07 [Bib_Time] => 2021-12-30 07:37:07 [KeysWordContens] => Advancing diagnosis and treatment of Niemann-Pick C disease through biomarker discovery, Niemann-Pick C, cholesterol, biomarkers, diagnosis, oxysterol, bile acids, Niemann-Pick C disease is a rare neurodegenerative, lysosomal storage disease caused by accumulation of unesterified cholesterol. Diagnosis of the disease is often delayed due to its rarity, the heterogeneous presentation, and the early non-specific symptoms. The discovery of disease-specific biomarkers—cholestane-3β,5α,6β-triol (C-triol), trihydroxycholanic acid glycinate (TCG) and N-palmitoyl-O-phosphocholineserine [PPCS, initially referred to as lysosphingomyelin-509 (lysoSM-509)]—has led to development of non-invasive, blood-based diagnostics. Dissemination of these rapid, sensitive, and specific clinical assays has accelerated diagnosis. Moreover, the superior receiver operating characteristic of the TCG bile acid biomarker and its detection in dried blood spots has also facilitated development of a newborn screen for NPC, which is currently being piloted in New York state. The C-triol, TCG and PPCS biomarkers have also been proved useful for monitoring treatment response in peripheral tissues, but are uninformative with respect to treatment efficacy in the central nervous system (CNS). A major gap for the field is the lack of a validated, non-invasive biomarker to monitor the course of disease and CNS response to therapy. ,Xuntian Jiang, Daniel S. Ory [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Xuntian Jiang, Daniel S. Ory ) [12] => Array ( [ArticleId] => 226 [Create_Time] => 2021-12-17 [zipUrl] => https://www.explorationpub.com/uploads/zip/202201/20220128080217.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100413/100413.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100413/100413.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100413/100413-cover.png [JournalsId] => 7 [Title] => Targeting cytochrome P450 46A1 and brain cholesterol 24-hydroxylation to treat neurodegenerative diseases [Abstract] => The brain cholesterol content is determined by the balance between the pathways of in situ biosynthesis and cholesterol elimination via 24-hydroxylation catalyzed by cytochrome P450 46A1 (CYP46A1). [AbstractComplete] =>

The brain cholesterol content is determined by the balance between the pathways of in situ biosynthesis and cholesterol elimination via 24-hydroxylation catalyzed by cytochrome P450 46A1 (CYP46A1). Both pathways are tightly coupled and determine the rate of brain cholesterol turnover. Evidence is accumulating that modulation of CYP46A1 activity by gene therapy or pharmacologic means could be beneficial in the case of neurodegenerative and other brain diseases and affect brain processes other than cholesterol biosynthesis and elimination. This minireview summarizes these other processes, most common of which include abnormal protein accumulation, memory, and cognition, motor behavior, gene transcription, protein phosphorylation as well as autophagy and lysosomal processing. The unifying mechanisms, by which these processes could be affected by CYP46A targeting are also discussed.

[Names] => Irina A. Pikuleva [CName] => Irina A.Pikuleva, [Doi] => 10.37349/ent.2021.00013 [Published] => December 30, 2021 [Viewed] => 2290 [Downloaded] => 87 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00013 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 44 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:159–172 [Recommend] => 0 [Keywords] => Cytochrome P450 46A1, 24-hydroxycholesterol, brain, cholesterol turnover, mevalonate pathway, sterol flux, acetyl-coenzyme A [DetailTitle] => Cholesterol Dyshomeostasis in Neurological Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/44 [Id] => 100413 [ris] => https://www.explorationpub.com/uploads/Article/A100413/b0578751ca3c87a7e07604499e45d899.ris [bib] => https://www.explorationpub.com/uploads/Article/A100413/05d869308a308a0dbffb7b1ccff2102f.bib [ens] => [Cited] => 4 [Cited_Time] => 2024-05-27 [CitethisArticle] => Pikuleva IA. Targeting cytochrome P450 46A1 and brain cholesterol 24-hydroxylation to treat neurodegenerative diseases. Explor Neuroprot Ther. 2021;1:159-72. https://doi.org/10.37349/ent.2021.00013 [Jindex] => 0 [CEmail] => iap8@case.edu, [Ris_Time] => 2021-12-30 08:05:01 [Bib_Time] => 2021-12-30 08:05:01 [KeysWordContens] => Targeting cytochrome P450 46A1 and brain cholesterol 24-hydroxylation to treat neurodegenerative diseases, Cytochrome P450 46A1, 24-hydroxycholesterol, brain, cholesterol turnover, mevalonate pathway, sterol flux, acetyl-coenzyme A, The brain cholesterol content is determined by the balance between the pathways of in situ biosynthesis and cholesterol elimination via 24-hydroxylation catalyzed by cytochrome P450 46A1 (CYP46A1). Both pathways are tightly coupled and determine the rate of brain cholesterol turnover. Evidence is accumulating that modulation of CYP46A1 activity by gene therapy or pharmacologic means could be beneficial in the case of neurodegenerative and other brain diseases and affect brain processes other than cholesterol biosynthesis and elimination. This minireview summarizes these other processes, most common of which include abnormal protein accumulation, memory, and cognition, motor behavior, gene transcription, protein phosphorylation as well as autophagy and lysosomal processing. The unifying mechanisms, by which these processes could be affected by CYP46A targeting are also discussed. ,Irina A. Pikuleva [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Irina A. Pikuleva ) [13] => Array ( [ArticleId] => 236 [Create_Time] => 2021-12-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202112/20211230093607.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100414/100414.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100414/100414.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100414/100414_cover.png [JournalsId] => 7 [Title] => Blocking cholesterol storage to treat Alzheimer’s disease [Abstract] => Cholesterol serves as an essential lipid molecule in various membrane organelles of mammalian cells. The metabolites of cholesterol also play important functions. Acyl-coenzyme A: cholesterol acyltr [AbstractComplete] =>

Cholesterol serves as an essential lipid molecule in various membrane organelles of mammalian cells. The metabolites of cholesterol also play important functions. Acyl-coenzyme A: cholesterol acyltransferase 1 (ACAT1), also named as sterol O-acyltransferase 1, is a membrane-bound enzyme residing at the endoplasmic reticulum (ER). It converts cholesterol to cholesteryl esters (CEs) for storage, and is expressed in all cells. CEs cannot partition in membranes; they can only coalesce as cytosolic lipid droplets. Excess CEs are found in the vulnerable region of the brains of patients with late-onset Alzheimer’s disease (AD), and in cell and mouse models for AD. Reducing CE contents by genetic inactivation of ACAT1, or by pharmacological inhibition of ACAT is shown to reduce amyloidopathy and other hallmarks for AD. To account for the various beneficial actions of the ACAT1 blockade (A1B), a working hypothesis is proposed here: the increase in CE contents observed in the AD brain is caused by damages of cholesterol-rich lipid rafts that are known to occur in neurons affected by AD. These damages cause cholesterol to release from lipid rafts and move to the ER where it will be converted to CEs by ACAT1. In addition, the increase in CE contents may also be caused by overloading with cholesterol-rich substances, or through activation of ACAT1 gene expression by various pro-inflammatory agents. Both scenarios may occur in microglia of the chronically inflamed brain. A1B ameliorates AD by diverting the cholesterol pool destined for CE biosynthesis such that it can be utilized more efficiently to repair membrane damage in various organelles, and to exert regulatory actions more effectively to defend against AD. To test the validity of the A1B hypothesis in cell culture and in vivo, the current status of various anti-ACAT1 agents that could be further developed is briefly discussed.

[Names] => Ta Yuan Chang ... James G. Gow [CName] => Ta YuanChang,Catherine C. Y.Chang, [Doi] => 10.37349/ent.2021.00014 [Published] => December 30, 2021 [Viewed] => 2820 [Downloaded] => 89 [Subject] => Review [Year] => 2021 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2021.00014 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 44 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2021;1:173–184 [Recommend] => 0 [Keywords] => Alzheimer’s disease, cholesterol acyltransferase, cholesterol [DetailTitle] => Cholesterol Dyshomeostasis in Neurological Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/44 [Id] => 100414 [ris] => https://www.explorationpub.com/uploads/Article/A100414/289b0793e914a121b2a176e1cd8b02a4.ris [bib] => https://www.explorationpub.com/uploads/Article/A100414/147a5126ef831edcb06c548d0f1625cb.bib [ens] => [Cited] => 12 [Cited_Time] => 2024-05-27 [CitethisArticle] => Chang TY, Chang CCY, Harned TC, De La Torre AL, Lee J, Huynh TN, et al. Blocking cholesterol storage to treat Alzheimer’s disease. Explor Neuroprot Ther. 2021;1:173-84. https://doi.org/10.37349/ent.2021.00014 [Jindex] => 0 [CEmail] => ta.yuan.chang@dartmouth.edu,catherine.chang@dartmouth.edu, [Ris_Time] => 2021-12-31 09:02:40 [Bib_Time] => 2021-12-31 09:02:40 [KeysWordContens] => Blocking cholesterol storage to treat Alzheimer’s disease, Alzheimer’s disease, cholesterol acyltransferase, cholesterol, Cholesterol serves as an essential lipid molecule in various membrane organelles of mammalian cells. The metabolites of cholesterol also play important functions. Acyl-coenzyme A: cholesterol acyltransferase 1 (ACAT1), also named as sterol O-acyltransferase 1, is a membrane-bound enzyme residing at the endoplasmic reticulum (ER). It converts cholesterol to cholesteryl esters (CEs) for storage, and is expressed in all cells. CEs cannot partition in membranes; they can only coalesce as cytosolic lipid droplets. Excess CEs are found in the vulnerable region of the brains of patients with late-onset Alzheimer’s disease (AD), and in cell and mouse models for AD. Reducing CE contents by genetic inactivation of ACAT1, or by pharmacological inhibition of ACAT is shown to reduce amyloidopathy and other hallmarks for AD. To account for the various beneficial actions of the ACAT1 blockade (A1B), a working hypothesis is proposed here: the increase in CE contents observed in the AD brain is caused by damages of cholesterol-rich lipid rafts that are known to occur in neurons affected by AD. These damages cause cholesterol to release from lipid rafts and move to the ER where it will be converted to CEs by ACAT1. In addition, the increase in CE contents may also be caused by overloading with cholesterol-rich substances, or through activation of ACAT1 gene expression by various pro-inflammatory agents. Both scenarios may occur in microglia of the chronically inflamed brain. A1B ameliorates AD by diverting the cholesterol pool destined for CE biosynthesis such that it can be utilized more efficiently to repair membrane damage in various organelles, and to exert regulatory actions more effectively to defend against AD. To test the validity of the A1B hypothesis in cell culture and in vivo, the current status of various anti-ACAT1 agents that could be further developed is briefly discussed. ,Ta Yuan Chang ... James G. Gow [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Ta Yuan Chang, Catherine C. Y. Chang, Taylor C. Harned, Adrianna L. De La Torre, Junghoon Lee, Thao N. Huynh, James G. Gow ) [14] => Array ( [ArticleId] => 242 [Create_Time] => 2022-01-06 [zipUrl] => https://www.explorationpub.com/uploads/zip/202205/20220519005416.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100415/100415.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100415/100415.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100415/100415_Cover.png [JournalsId] => 7 [Title] => Balancing cholesterol in the brain: from synthesis to disposal [Abstract] => The cholesterol is a vital component of cell membranes and myelin sheaths, and a precursor for essential molecules such as steroid hormones. In humans, cholesterol is partially obtained through the [AbstractComplete] =>

The cholesterol is a vital component of cell membranes and myelin sheaths, and a precursor for essential molecules such as steroid hormones. In humans, cholesterol is partially obtained through the diet, while the majority is synthesized in the body, primarily in the liver. However, the limited exchange between the central nervous system and peripheral circulation, due to the presence of the blood-brain barrier, necessitates cholesterol in the brain to be exclusively acquired from local de novo synthesis. This cholesterol is reutilized efficiently, rendering a much slower overall turnover of the compound in the brain as compared with the periphery. Furthermore, brain cholesterol is regulated independently from peripheral cholesterol. Numerous enzymes, proteins, and other factors are involved in cholesterol synthesis and metabolism in the brain. Understanding the unique mechanisms and pathways involved in the maintenance of cholesterol homeostasis in the brain is critical, considering perturbations to these processes are implicated in numerous neurodegenerative diseases. This review focuses on the developing understanding of cholesterol metabolism in the brain, discussing the sites and processes involved in its synthesis and regulation, as well as the mechanisms involved in its distribution throughout, and elimination from, the brain.

[Names] => Lydia Qian ... Andrew J. Brown [CName] => Ingrid C.Gelissen,Andrew J.Brown, [Doi] => 10.37349/ent.2022.00015 [Published] => January 05, 2022 [Viewed] => 6088 [Downloaded] => 310 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00015 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 44 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:1–27 [Recommend] => 0 [Keywords] => Brain, cholesterol synthesis, cholesterol disposal, oxysterols, ATP-binding cassette transporters, apolipoproteins [DetailTitle] => Cholesterol Dyshomeostasis in Neurological Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/44 [Id] => 100415 [ris] => https://www.explorationpub.com/uploads/Article/A100415/1cf1a9e24c17c6c1e9c0d8a48d6818b4.ris [bib] => https://www.explorationpub.com/uploads/Article/A100415/aa5cfe3bf7291e2d51cb71d0f3766e6b.bib [ens] => [Cited] => 8 [Cited_Time] => 2024-05-27 [CitethisArticle] => Qian L, Chai AB, Gelissen IC, Brown AJ. Balancing cholesterol in the brain: from synthesis to disposal. Explor Neuroprot Ther. 2022;2:1-27. https://doi.org/10.37349/ent.2022.00015 [Jindex] => 0 [CEmail] => ingrid.gelissen@sydney.edu.au,aj.brown@unsw.edu.au, [Ris_Time] => 2022-01-21 03:32:02 [Bib_Time] => 2022-01-21 03:32:02 [KeysWordContens] => Balancing cholesterol in the brain: from synthesis to disposal, Brain, cholesterol synthesis, cholesterol disposal, oxysterols, ATP-binding cassette transporters, apolipoproteins, The cholesterol is a vital component of cell membranes and myelin sheaths, and a precursor for essential molecules such as steroid hormones. In humans, cholesterol is partially obtained through the diet, while the majority is synthesized in the body, primarily in the liver. However, the limited exchange between the central nervous system and peripheral circulation, due to the presence of the blood-brain barrier, necessitates cholesterol in the brain to be exclusively acquired from local de novo synthesis. This cholesterol is reutilized efficiently, rendering a much slower overall turnover of the compound in the brain as compared with the periphery. Furthermore, brain cholesterol is regulated independently from peripheral cholesterol. Numerous enzymes, proteins, and other factors are involved in cholesterol synthesis and metabolism in the brain. Understanding the unique mechanisms and pathways involved in the maintenance of cholesterol homeostasis in the brain is critical, considering perturbations to these processes are implicated in numerous neurodegenerative diseases. This review focuses on the developing understanding of cholesterol metabolism in the brain, discussing the sites and processes involved in its synthesis and regulation, as well as the mechanisms involved in its distribution throughout, and elimination from, the brain. ,Lydia Qian ... Andrew J. Brown [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Lydia Qian, Amanda B. Chai, Ingrid C. Gelissen, Andrew J. Brown ) [15] => Array ( [ArticleId] => 258 [Create_Time] => 2022-02-17 [zipUrl] => https://www.explorationpub.com/uploads/zip/202202/20220217080806.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100416/100416.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100416/100416.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100416/100416_cover.png [JournalsId] => 7 [Title] => Dry needling in stroke [Abstract] => Stroke causes acute neurological deficit which is an important cause of morbidity and mortality. Neurorehabilitation is an important dimension in the management of post-stroke deficits. Spasticity, [AbstractComplete] =>

Stroke causes acute neurological deficit which is an important cause of morbidity and mortality. Neurorehabilitation is an important dimension in the management of post-stroke deficits. Spasticity, pain, and neurological deficits are contributors to post-stroke disability. Dry needling (DN) is a technique commonly used in the management of myofascial pain. Recent evidence suggests its efficacy in the management of post-stroke disability. The descriptive review on the use of DN summarises the evidence for the management of post-stroke patients such as spasticity, balance, pain, functional outcome, tremor, and ultrasonographic evidence. The filiform needle is inserted into the target muscle until a local twitch response is obtained. The effects of DN are produced by the local stretch of the spastic muscle and afferent modulation of the reflex arc that decreases the excitability of the alpha motor neuron. The DN reduces muscle spasticity in post-stroke patients. The improved spasticity is translated to better functional outcomes and balance. The procedure is also shown to reduce pain including post-stroke shoulder pain. It is also shown to improve tremors in post-stroke patients. Ultrasonographic evidence of the beneficial effects of DN shows improved measures in the pennate angle and mean muscle thickness. Concurrent use of DN and electrical stimulation improve spasticity, the effect which may be seen for longer periods. DN is emerging as a useful and cost-effective technique in the management of post-stroke patients. The evidence for the use of DN in the management of post-stroke spasticity is high. However, more research is required to assess its efficacy in functional outcomes and other aspects of the stroke.

[Names] => Nirmal Surya, Guhan Ramamurthy [CName] => [Doi] => 10.37349/ent.2022.00016 [Published] => February 17, 2022 [Viewed] => 3230 [Downloaded] => 99 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00016 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 57 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:28–35 [Recommend] => 0 [Keywords] => Dry needling, spasticity, post-stroke pain, balance [DetailTitle] => Dry Needling for Neurological Disorders [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/57 [Id] => 100416 [ris] => https://www.explorationpub.com/uploads/Article/A100416/86aa616cabc0488c08d2fd83ff42023b.ris [bib] => https://www.explorationpub.com/uploads/Article/A100416/ff6f9cf0073ef89e35b530489d815b25.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Surya N, Ramamurthy G. Dry needling in stroke. Explor Neuroprot Ther. 2022;2:28–35. https://doi.org/10.37349/ent.2022.00016 [Jindex] => 0 [CEmail] => [Ris_Time] => 2022-02-17 07:14:13 [Bib_Time] => 2022-02-17 07:14:13 [KeysWordContens] => Dry needling in stroke, Dry needling, spasticity, post-stroke pain, balance, Stroke causes acute neurological deficit which is an important cause of morbidity and mortality. Neurorehabilitation is an important dimension in the management of post-stroke deficits. Spasticity, pain, and neurological deficits are contributors to post-stroke disability. Dry needling (DN) is a technique commonly used in the management of myofascial pain. Recent evidence suggests its efficacy in the management of post-stroke disability. The descriptive review on the use of DN summarises the evidence for the management of post-stroke patients such as spasticity, balance, pain, functional outcome, tremor, and ultrasonographic evidence. The filiform needle is inserted into the target muscle until a local twitch response is obtained. The effects of DN are produced by the local stretch of the spastic muscle and afferent modulation of the reflex arc that decreases the excitability of the alpha motor neuron. The DN reduces muscle spasticity in post-stroke patients. The improved spasticity is translated to better functional outcomes and balance. The procedure is also shown to reduce pain including post-stroke shoulder pain. It is also shown to improve tremors in post-stroke patients. Ultrasonographic evidence of the beneficial effects of DN shows improved measures in the pennate angle and mean muscle thickness. Concurrent use of DN and electrical stimulation improve spasticity, the effect which may be seen for longer periods. DN is emerging as a useful and cost-effective technique in the management of post-stroke patients. The evidence for the use of DN in the management of post-stroke spasticity is high. However, more research is required to assess its efficacy in functional outcomes and other aspects of the stroke. ,Nirmal Surya, Guhan Ramamurthy [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Nirmal Surya, Guhan Ramamurthy ) [16] => Array ( [ArticleId] => 261 [Create_Time] => 2022-02-23 [zipUrl] => https://www.explorationpub.com/uploads/zip/202204/20220418090842.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100417/100417.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100417/100417.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100417/100417_cover.png [JournalsId] => 7 [Title] => Various facets of excitotoxicity [Abstract] => Aim: Excitotoxicity results from unusually increased activation of excitatory amino acid receptors leading to neuronal death. Since glutamate is the main excitatory neurotransmitter in the centra [AbstractComplete] =>

Aim:

Excitotoxicity results from unusually increased activation of excitatory amino acid receptors leading to neuronal death. Since glutamate is the main excitatory neurotransmitter in the central nervous system, it is also the most common excitotoxicity trigger. This uncontrolled neuronal response participates in various neurodegenerative diseases, such as ischemia, hypoglycemia, Huntington’s, Parkinson’s and Alzheimer’s disease. Thus, the investigation in the field expanded a lot in the past decade, leading to in vitro modelling adaptations. However, much performed work on glutamate-induced excitotoxicity is methodologically inconsistent in the literature. The field lacks reproducibility, which is one of the main fundaments of empirical science. In this regard, the literature was summarized and the main methodological features were critically evaluated, aiming to guide the researchers that are starting in the field.

Methods:

Published data since 1985 from PUBMED were collected and analyzed to observe which in vitro experimental conditions of excitotoxicity were reproducible. The suggested methods were based on the characteristics of excitotoxicity, such as abnormal intracellular calcium mediated signaling, mitochondria impairment, reactive oxygen species accumulation and cell death. Various conditions and comparative controls were used to design the standard investigation of excitotoxicity, such as culture medium content (presence of glutamate and aspartate), time interval of induction and the concentration of the inductor, based on the most reproducible published ones.

Results:

Our results and critical analysis point to some experimental conditions to consider, such as primary cultured neurons are more sensitive to glutamate and the response obtained is more robust than in other models; excitotoxicity mediated effects are better observed one hour following the stimulus; the culture medium should contain low levels of glutamate or aspartate or glycine. Online available phosphoproteomic data on excitotoxicity using the primary cortical neurons in vitro model supported the same conditions proposed by us.

Conclusions:

This manuscript will facilitate the design of any research for excitotoxic or neuroprotective compounds in physiological and pathophysiological conditions by standardizing and improving experimental conditions.

[Names] => Talita Glaser ... Henning Ulrich [CName] => HenningUlrich, [Doi] => 10.37349/ent.2022.00017 [Published] => February 23, 2022 [Viewed] => 4152 [Downloaded] => 153 [Subject] => Systematic Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00017 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:36–64 [Recommend] => 0 [Keywords] => Glutamate, cell death, calcium, mitochondria, neurodegeneration [DetailTitle] => [DetailUrl] => [Id] => 100417 [ris] => https://www.explorationpub.com/uploads/Article/A100417/51ecbc3605621fdd8758b6f6d9c633f4.ris [bib] => https://www.explorationpub.com/uploads/Article/A100417/9354d5fd6b2b236a116344739b2fe190.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-05-27 [CitethisArticle] => Glaser T, Silva JB, Juvenal GA, Maiolini PN, Turrini N, Petiz LL, et al. Various facets of excitotoxicity. Explor Neuroprot Ther. 2022;2:36–64. https://doi.org/10.37349/ent.2022.00017 [Jindex] => 0 [CEmail] => henning@iq.usp.br, [Ris_Time] => 2022-02-23 06:45:15 [Bib_Time] => 2022-02-23 07:26:45 [KeysWordContens] => Various facets of excitotoxicity, Glutamate, cell death, calcium, mitochondria, neurodegeneration, Aim: Excitotoxicity results from unusually increased activation of excitatory amino acid receptors leading to neuronal death. Since glutamate is the main excitatory neurotransmitter in the central nervous system, it is also the most common excitotoxicity trigger. This uncontrolled neuronal response participates in various neurodegenerative diseases, such as ischemia, hypoglycemia, Huntington’s, Parkinson’s and Alzheimer’s disease. Thus, the investigation in the field expanded a lot in the past decade, leading to in vitro modelling adaptations. However, much performed work on glutamate-induced excitotoxicity is methodologically inconsistent in the literature. The field lacks reproducibility, which is one of the main fundaments of empirical science. In this regard, the literature was summarized and the main methodological features were critically evaluated, aiming to guide the researchers that are starting in the field. Methods: Published data since 1985 from PUBMED were collected and analyzed to observe which in vitro experimental conditions of excitotoxicity were reproducible. The suggested methods were based on the characteristics of excitotoxicity, such as abnormal intracellular calcium mediated signaling, mitochondria impairment, reactive oxygen species accumulation and cell death. Various conditions and comparative controls were used to design the standard investigation of excitotoxicity, such as culture medium content (presence of glutamate and aspartate), time interval of induction and the concentration of the inductor, based on the most reproducible published ones. Results: Our results and critical analysis point to some experimental conditions to consider, such as primary cultured neurons are more sensitive to glutamate and the response obtained is more robust than in other models; excitotoxicity mediated effects are better observed one hour following the stimulus; the culture medium should contain low levels of glutamate or aspartate or glycine. Online available phosphoproteomic data on excitotoxicity using the primary cortical neurons in vitro model supported the same conditions proposed by us. Conclusions: This manuscript will facilitate the design of any research for excitotoxic or neuroprotective compounds in physiological and pathophysiological conditions by standardizing and improving experimental conditions. ,Talita Glaser ... Henning Ulrich [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Talita Glaser, Jean Bezerra Silva, Guilherme A. Juvenal, Pedro Negrão Maiolini, Natalia Turrini, Lyvia Lintzmaier Petiz, Lucas Bonfim Marques, Deidiane Elisa Ribeiro, Qing Ye, Yong Tang, Henning Ulrich ) [17] => Array ( [ArticleId] => 275 [Create_Time] => 2022-03-02 [zipUrl] => https://www.explorationpub.com/uploads/zip/202205/20220511070806.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100418/100418.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100418/100418.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100418/100418_cover.png [JournalsId] => 7 [Title] => Subarachnoid hemorrhage: management considerations for COVID-19 [Abstract] => Subarachnoid hemorrhage (SAH) has deleterious outcomes for patients, and during the hospital stay, patients are susceptible to vasospasm and delayed cerebral ischemia. Coronavirus disease 2019 (COVI [AbstractComplete] =>

Subarachnoid hemorrhage (SAH) has deleterious outcomes for patients, and during the hospital stay, patients are susceptible to vasospasm and delayed cerebral ischemia. Coronavirus disease 2019 (COVID-19) has been shown to worsen hypertension through angiotensin-converting enzyme 2 (ACE2) activity, therefore, predisposing to aneurysm rupture. The classic renin-angiotensin pathway activation also predisposes to vasospasm and subsequent delayed cerebral ischemia. Matrix metalloproteinase 9 upregulation can lead to an inflammatory surge, which worsens outcomes for patients. SAH patients with COVID-19 are more susceptible to ventilator-associated pneumonia, reversible cerebral vasoconstriction syndrome, and respiratory distress. Emerging treatments are warranted to target key components of the anti-inflammatory cascade. The aim of this review is to explore how the COVID-19 virus and the intensive care unit (ICU) treatment of severe COVID can contribute to SAH.

Broad effects of COVID-19 on inducing SAH. Created with BioRender.com. RBC: red blood cell; MMP-9: matrix metalloproteinase 9

[Names] => Eric J. Panther, Brandon Lucke-Wold [CName] => BrandonLucke-Wold, [Doi] => 10.37349/ent.2022.00018 [Published] => March 02, 2022 [Viewed] => 3434 [Downloaded] => 60 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00018 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 66 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:65–73 [Recommend] => 1 [Keywords] => Subarachnoid hemorrhage, COVID-19, renin-angiotensin pathway, matrix metalloproteinase 9, outcomes [DetailTitle] => Emerging Concepts in Subarachnoid Hemorrhage [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/66 [Id] => 100418 [ris] => https://www.explorationpub.com/uploads/Article/A100418/0e83ad8cd2246c1d2e378dc2f313cb08.ris [bib] => https://www.explorationpub.com/uploads/Article/A100418/4a499b0d6b05b4ca0a2dfe8c6aac31e1.bib [ens] => [Cited] => 11 [Cited_Time] => 2024-05-27 [CitethisArticle] => Panther EJ, Lucke-Wold B. Subarachnoid hemorrhage: management considerations for COVID-19. Explor Neuroprot Ther. 2022;2:65–73. https://doi.org/10.37349/ent.2022.00018 [Jindex] => 0 [CEmail] => Brandon.Lucke-Wold@neurosurgery.ufl.edu, [Ris_Time] => 2022-03-02 07:27:40 [Bib_Time] => 2022-03-02 07:27:40 [KeysWordContens] => Subarachnoid hemorrhage: management considerations for COVID-19, Subarachnoid hemorrhage, COVID-19, renin-angiotensin pathway, matrix metalloproteinase 9, outcomes, Subarachnoid hemorrhage (SAH) has deleterious outcomes for patients, and during the hospital stay, patients are susceptible to vasospasm and delayed cerebral ischemia. Coronavirus disease 2019 (COVID-19) has been shown to worsen hypertension through angiotensin-converting enzyme 2 (ACE2) activity, therefore, predisposing to aneurysm rupture. The classic renin-angiotensin pathway activation also predisposes to vasospasm and subsequent delayed cerebral ischemia. Matrix metalloproteinase 9 upregulation can lead to an inflammatory surge, which worsens outcomes for patients. SAH patients with COVID-19 are more susceptible to ventilator-associated pneumonia, reversible cerebral vasoconstriction syndrome, and respiratory distress. Emerging treatments are warranted to target key components of the anti-inflammatory cascade. The aim of this review is to explore how the COVID-19 virus and the intensive care unit (ICU) treatment of severe COVID can contribute to SAH. Graphical abstract. Broad effects of COVID-19 on inducing SAH. Created with BioRender.com. RBC: red blood cell; MMP-9: matrix metalloproteinase 9 ,Eric J. Panther, Brandon Lucke-Wold [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Eric J. Panther, Brandon Lucke-Wold ) [18] => Array ( [ArticleId] => 298 [Create_Time] => 2022-04-25 [zipUrl] => https://www.explorationpub.com/uploads/zip/202204/20220425005508.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100419/100419.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100419/100419.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100419/100419_cover.png [JournalsId] => 7 [Title] => Gut microbiota could modulate the effects of neuro-immune responses and memory traces via the gut-brain-immune axis in schizophrenia [Abstract] => Altered immunity may have destructive consequences for the integrated central nervous system. This immune response often affects progressive neurodegenerative diseases such as Parkinson’s disease and/or psychiatric disorders such as schizophrenia. In particular, schizophrenia pathogenesis may be mediated by multiple neuro-immune interaction pathways. Gut microbiota might affect the brain and/or immune function. Significant machineries of immunity are commonly affected by the commensal gut microbiota. Therefore, schizophrenia may be connected with the gut-immune system. In addition, the brain and immune systems cooperate on multiple levels. The brain could save several pieces of information about specific inflammation in a body. This immunological memory named “engrams”, also called memory traces, could restore the initial disease state, which may help to explain key features of schizophrenia. Based on this concept, therapeutic strategies for schizophrenia could be the modification of the gut microbiota. Probiotics and/or fecal microbiota transplantation are now emerging as the most promising treatments for the modification. More consideration of the roles of gut microbiota will conduct the further development of immune-based therapeutics for the prevention and/or treatments of psychiatric disorders. [AbstractComplete] =>

Altered immunity may have destructive consequences for the integrated central nervous system. This immune response often affects progressive neurodegenerative diseases such as Parkinson’s disease and/or psychiatric disorders such as schizophrenia. In particular, schizophrenia pathogenesis may be mediated by multiple neuro-immune interaction pathways. Gut microbiota might affect the brain and/or immune function. Significant machineries of immunity are commonly affected by the commensal gut microbiota. Therefore, schizophrenia may be connected with the gut-immune system. In addition, the brain and immune systems cooperate on multiple levels. The brain could save several pieces of information about specific inflammation in a body. This immunological memory named “engrams”, also called memory traces, could restore the initial disease state, which may help to explain key features of schizophrenia. Based on this concept, therapeutic strategies for schizophrenia could be the modification of the gut microbiota. Probiotics and/or fecal microbiota transplantation are now emerging as the most promising treatments for the modification. More consideration of the roles of gut microbiota will conduct the further development of immune-based therapeutics for the prevention and/or treatments of psychiatric disorders.

[Names] => Haruka Sawamura ... Satoru Matsuda [CName] => [Doi] => 10.37349/ent.2022.00019 [Published] => April 24, 2022 [Viewed] => 5924 [Downloaded] => 1809 [Subject] => Perspective [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00019 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 55 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:74–86 [Recommend] => 0 [Keywords] => Gut microbiota, short-chain fatty acids, engram, schizophrenia, inflammation, reactive oxygen species [DetailTitle] => Intervention of Neuroimmune Responses [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/55 [Id] => 100419 [ris] => https://www.explorationpub.com/uploads/Article/A100419/b9dbf1fafef032e18271fc1cb9051b42.ris [bib] => https://www.explorationpub.com/uploads/Article/A100419/6e1abaeabab7e7b4b0bdc1aafa815333.bib [ens] => [Cited] => 3 [Cited_Time] => 2024-05-27 [CitethisArticle] => Sawamura H, Taniguchi K, Ikeda Y, Tsuji A, Kitagishi Y, Matsuda S. Gut microbiota could modulate the effects of neuro-immune responses and memory traces via the gut-brain-immune axis in schizophrenia. Explor Neuroprot Ther. 2022;2:74–86. https://doi.org/10.37349/ent.2022.00019 [Jindex] => 0 [CEmail] => [Ris_Time] => 2022-04-25 00:49:11 [Bib_Time] => 2022-04-25 00:49:11 [KeysWordContens] => Gut microbiota could modulate the effects of neuro-immune responses and memory traces via the gut-brain-immune axis in schizophrenia, Gut microbiota, short-chain fatty acids, engram, schizophrenia, inflammation, reactive oxygen species, Altered immunity may have destructive consequences for the integrated central nervous system. This immune response often affects progressive neurodegenerative diseases such as Parkinson’s disease and/or psychiatric disorders such as schizophrenia. In particular, schizophrenia pathogenesis may be mediated by multiple neuro-immune interaction pathways. Gut microbiota might affect the brain and/or immune function. Significant machineries of immunity are commonly affected by the commensal gut microbiota. Therefore, schizophrenia may be connected with the gut-immune system. In addition, the brain and immune systems cooperate on multiple levels. The brain could save several pieces of information about specific inflammation in a body. This immunological memory named “engrams”, also called memory traces, could restore the initial disease state, which may help to explain key features of schizophrenia. Based on this concept, therapeutic strategies for schizophrenia could be the modification of the gut microbiota. Probiotics and/or fecal microbiota transplantation are now emerging as the most promising treatments for the modification. More consideration of the roles of gut microbiota will conduct the further development of immune-based therapeutics for the prevention and/or treatments of psychiatric disorders. ,Haruka Sawamura ... Satoru Matsuda [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Haruka Sawamura, Kurumi Taniguchi, Yuka Ikeda, Ai Tsuji, Yasuko Kitagishi, Satoru Matsuda ) [19] => Array ( [ArticleId] => 307 [Create_Time] => 2022-04-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230613065939.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100420/100420.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100420/100420.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100420/100420_cover.png [JournalsId] => 7 [Title] => The role of physical activity against chemotherapy-induced peripheral neuropathy: a narrative review [Abstract] => Several studies investigated the side effect of adjuvant cancer treatments, and different types of preventive techniques or treatments have been assessed. Chemotherapy-induced peripheral neuropathy [AbstractComplete] =>

Several studies investigated the side effect of adjuvant cancer treatments, and different types of preventive techniques or treatments have been assessed. Chemotherapy-induced peripheral neuropathy (CIPN) is the most common neurological side effect. Exercise training has been widely studied as an adjuvant therapy to prevent CIPN and improve post-chemotherapy functional outcome and quality of life (QoL). This narrative review aims to summarize the data obtained from the latest studies about physical activity (PA) for the prevention and treatment of CIPN and associated QoL measures. Literature research was conducted to obtain studies including PA interventions for patients with CIPN. Ten studies met inclusion criteria and were therefore summarized and discussed, focusing on exercise type and functional outcome. It seems clear that, regardless of the type of exercise, PA plays a positive role in the treatment of CIPN, providing a significant symptom improvement. There has been no standardization of type, quantity, and intensity of PA administered to the subjects in the various studies probably due to a physiological difference between samples, grade of neuropathy, and difference among therapies.

[Names] => Daniele Diotti ... Lucio Marinelli [CName] => LucioMarinelli, [Doi] => 10.37349/ent.2022.00020 [Published] => April 28, 2022 [Viewed] => 1928 [Downloaded] => 86 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00020 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:87–99 [Recommend] => 0 [Keywords] => Chemotherapy-induced peripheral neuropathy, cancer, physical activity, treatment, prevention [DetailTitle] => [DetailUrl] => [Id] => 100420 [ris] => https://www.explorationpub.com/uploads/Article/A100420/0e0648112ce8e1cc87147a65f0d1d782.ris [bib] => https://www.explorationpub.com/uploads/Article/A100420/79d08ac07ca59bf599e16482c4b8fcc3.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-05-26 [CitethisArticle] => Diotti D, Puce L, Mori L, Trompetto C, Saretti E, Contenti C, et al. The role of physical activity against chemotherapy-induced peripheral neuropathy: a narrative review. Explor Neuroprot Ther. 2022;2:87–99. https://doi.org/10.37349/ent.2022.00020 [Jindex] => 0 [CEmail] => lucio.marinelli@unige.it, [Ris_Time] => 2022-04-28 00:38:38 [Bib_Time] => 2022-04-28 00:38:38 [KeysWordContens] => The role of physical activity against chemotherapy-induced peripheral neuropathy: a narrative review, Chemotherapy-induced peripheral neuropathy, cancer, physical activity, treatment, prevention, Several studies investigated the side effect of adjuvant cancer treatments, and different types of preventive techniques or treatments have been assessed. Chemotherapy-induced peripheral neuropathy (CIPN) is the most common neurological side effect. Exercise training has been widely studied as an adjuvant therapy to prevent CIPN and improve post-chemotherapy functional outcome and quality of life (QoL). This narrative review aims to summarize the data obtained from the latest studies about physical activity (PA) for the prevention and treatment of CIPN and associated QoL measures. Literature research was conducted to obtain studies including PA interventions for patients with CIPN. Ten studies met inclusion criteria and were therefore summarized and discussed, focusing on exercise type and functional outcome. It seems clear that, regardless of the type of exercise, PA plays a positive role in the treatment of CIPN, providing a significant symptom improvement. There has been no standardization of type, quantity, and intensity of PA administered to the subjects in the various studies probably due to a physiological difference between samples, grade of neuropathy, and difference among therapies. ,Daniele Diotti ... Lucio Marinelli [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Daniele Diotti, Luca Puce, Laura Mori, Carlo Trompetto, Elena Saretti, Cecilia Contenti, Lucio Marinelli ) [20] => Array ( [ArticleId] => 323 [Create_Time] => 2022-06-20 [zipUrl] => https://www.explorationpub.com/uploads/zip/202206/20220620093946.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100421/100421.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100421/100421.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100421/100421_cover.png [JournalsId] => 7 [Title] => Combined effects of dry needling and exercises therapy on muscle spasticity and motor function in chronic stroke: a pretest-posttest pilot study [Abstract] => Aim: Spasticity is one of the most common symptoms in post-stroke patients. Dry needling (DN) is a relatively new method for the management of muscle spasticity. A multimodal treatment may be mor [AbstractComplete] =>

Aim:

Spasticity is one of the most common symptoms in post-stroke patients. Dry needling (DN) is a relatively new method for the management of muscle spasticity. A multimodal treatment may be more effective in spasticity management. The purpose of this study was to explore the short-term combined effects of DN and exercise therapy on wrist flexor spasticity, motor function, and motor neuron excitability in patients with chronic stroke.

Methods:

Ten patients with stroke and a mean age of 52 ± 4.9 years participated in this pretest-posttest pilot study. Patients received four sessions of DN and exercise therapy. Affected flexor carpi radialis and flexor carpi ulnaris muscles were needled each for 1 min. Patients underwent exercise therapy for about 30 min, once a week after DN. The outcome measures were the Modified Modified Ashworth Scale (MMAS), the maximal amplitude of H wave/maximal amplitude of M wave ratio (Hmax/Mmax Ratio), H-reflex latency, wrist extension active and passive range of motion (ROM), Action Research Arm Test (ARAT), and Fugl-Meyer Assessment (FMA). Assessments were performed at baseline, after four sessions of treatment, and three weeks after treatment.

Results:

After treatment, significant improvements in MMAS, wrist passive ROM, ARAT, and FMA were obtained (P ≤ 0.05).

Conclusions:

DN combined with exercise therapy improved muscle spasticity and motor function in patients with chronic stroke. Further investigations with a randomized controlled trial design with a comparator group of DN only are warranted (https://www.irct.ir/ identifier: IRCT20180611040061N1).

[Names] => Seyedeh Saeideh Babazadeh-Zavieh ... Korosh Mansoori [CName] => [Doi] => 10.37349/ent.2022.00021 [Published] => June 20, 2022 [Viewed] => 1356 [Downloaded] => 56 [Subject] => Original Article [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00021 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 57 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:100–109 [Recommend] => 0 [Keywords] => Stroke, spasticity, dry needling, exercise therapy, Hoffmann reflex [DetailTitle] => Dry Needling for Neurological Disorders [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/57 [Id] => 100421 [ris] => https://www.explorationpub.com/uploads/Article/A100421/deefda3f838a732a0d058c699cd38d44.ris [bib] => https://www.explorationpub.com/uploads/Article/A100421/321f3bac7563589076e49f26dc76e163.bib [ens] => [Cited] => 4 [Cited_Time] => 2024-05-24 [CitethisArticle] => Babazadeh-Zavieh SS, Ansari NN, Ghotbi N, Naghdi S, Haeri SMJ, Khanmohammadi M, et al. Combined effects of dry needling and exercises therapy on muscle spasticity and motor function in chronic stroke: a pretest-posttest pilot study. Explor Neuroprot Ther. 2022;2:100–9. https://doi.org/10.37349/ent.2022.00021 [Jindex] => 0 [CEmail] => [Ris_Time] => 2022-06-20 06:34:05 [Bib_Time] => 2022-06-20 06:34:05 [KeysWordContens] => Combined effects of dry needling and exercises therapy on muscle spasticity and motor function in chronic stroke: a pretest-posttest pilot study, Stroke, spasticity, dry needling, exercise therapy, Hoffmann reflex, Aim: Spasticity is one of the most common symptoms in post-stroke patients. Dry needling (DN) is a relatively new method for the management of muscle spasticity. A multimodal treatment may be more effective in spasticity management. The purpose of this study was to explore the short-term combined effects of DN and exercise therapy on wrist flexor spasticity, motor function, and motor neuron excitability in patients with chronic stroke. Methods: Ten patients with stroke and a mean age of 52 ± 4.9 years participated in this pretest-posttest pilot study. Patients received four sessions of DN and exercise therapy. Affected flexor carpi radialis and flexor carpi ulnaris muscles were needled each for 1 min. Patients underwent exercise therapy for about 30 min, once a week after DN. The outcome measures were the Modified Modified Ashworth Scale (MMAS), the maximal amplitude of H wave/maximal amplitude of M wave ratio (Hmax/Mmax Ratio), H-reflex latency, wrist extension active and passive range of motion (ROM), Action Research Arm Test (ARAT), and Fugl-Meyer Assessment (FMA). Assessments were performed at baseline, after four sessions of treatment, and three weeks after treatment. Results: After treatment, significant improvements in MMAS, wrist passive ROM, ARAT, and FMA were obtained (P ≤ 0.05). Conclusions: DN combined with exercise therapy improved muscle spasticity and motor function in patients with chronic stroke. Further investigations with a randomized controlled trial design with a comparator group of DN only are warranted (https://www.irct.ir/ identifier: IRCT20180611040061N1). ,Seyedeh Saeideh Babazadeh-Zavieh ... Korosh Mansoori [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Seyedeh Saeideh Babazadeh-Zavieh, Noureddin Nakhostin Ansari, Nastaran Ghotbi, Soofia Naghdi, Seyed Mohammad Jafar Haeri, Mohammadreza Khanmohammadi, Korosh Mansoori ) [21] => Array ( [ArticleId] => 326 [Create_Time] => 2022-06-21 [zipUrl] => https://www.explorationpub.com/uploads/zip/202206/20220630060259.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100422/100422.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100422/100422.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100422/100422_cover.png [JournalsId] => 7 [Title] => Can meditation-based approaches improve the cleansing power of the glymphatic system? [Abstract] => The glymphatic system, first described in 2012, is a brain-wide perivascular network that plays an important role in promoting interstitial metabolic waste removal from the brain. Glymphatic pathway [AbstractComplete] =>

The glymphatic system, first described in 2012, is a brain-wide perivascular network that plays an important role in promoting interstitial metabolic waste removal from the brain. Glymphatic pathway function has been reported to be dramatically diminished in the aging brain. Furthermore, glymphatic system dysfunction has been linked to a spectrum of neurodegenerative diseases including Alzheimer’s disease (AD). This waste clearance pathway of the brain is most active during sleep and is largely disengaged during wakefulness. While norepinephrine (NE) is responsible for suppressing the glymphatic function, electroencephalographic slow-wave (delta) activity has a facilitating effect. An intriguing question is whether these regulators of glymphatic activity can be modulated by meditation-based approaches and whether such approaches have the ability to increase glymphatic function in the awake brain. The present article hypothesizes that meditation-based approaches, such as immersive sound meditation, may have the potential to enhance glymphatic pathway transport and solute clearance by reducing NE and increasing slow-wave activity. If confirmed, meditation could be an attractive approach to promoting healthy brain aging and to preventing neurodegenerative conditions like AD.

[Names] => Peter Wostyn, Piet Goddaer [CName] => PeterWostyn, [Doi] => 10.37349/ent.2022.00022 [Published] => June 20, 2022 [Viewed] => 2682 [Downloaded] => 84 [Subject] => Perspective [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00022 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:110–117 [Recommend] => 0 [Keywords] => Aging, Alzheimer’s disease, glymphatic system, immersive sound, meditation, neurodegenerative disorders, norepinephrine, slow-wave activity [DetailTitle] => [DetailUrl] => [Id] => 100422 [ris] => https://www.explorationpub.com/uploads/Article/A100422/f0ecdddb33f568f815f3b16f5cdaf9a5.ris [bib] => https://www.explorationpub.com/uploads/Article/A100422/ea00df637f2c358044d70f67782abb01.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-05-27 [CitethisArticle] => Wostyn P, Goddaer P. Can meditation-based approaches improve the cleansing power of the glymphatic system? Explor Neuroprot Ther. 2022;2:110–7. https://doi.org/10.37349/ent.2022.00022 [Jindex] => 0 [CEmail] => wostyn.peter@skynet.be, [Ris_Time] => 2022-06-17 03:24:48 [Bib_Time] => 2022-06-17 03:24:48 [KeysWordContens] => Can meditation-based approaches improve the cleansing power of the glymphatic system? , Aging, Alzheimer’s disease, glymphatic system, immersive sound, meditation, neurodegenerative disorders, norepinephrine, slow-wave activity, The glymphatic system, first described in 2012, is a brain-wide perivascular network that plays an important role in promoting interstitial metabolic waste removal from the brain. Glymphatic pathway function has been reported to be dramatically diminished in the aging brain. Furthermore, glymphatic system dysfunction has been linked to a spectrum of neurodegenerative diseases including Alzheimer’s disease (AD). This waste clearance pathway of the brain is most active during sleep and is largely disengaged during wakefulness. While norepinephrine (NE) is responsible for suppressing the glymphatic function, electroencephalographic slow-wave (delta) activity has a facilitating effect. An intriguing question is whether these regulators of glymphatic activity can be modulated by meditation-based approaches and whether such approaches have the ability to increase glymphatic function in the awake brain. The present article hypothesizes that meditation-based approaches, such as immersive sound meditation, may have the potential to enhance glymphatic pathway transport and solute clearance by reducing NE and increasing slow-wave activity. If confirmed, meditation could be an attractive approach to promoting healthy brain aging and to preventing neurodegenerative conditions like AD. ,Peter Wostyn, Piet Goddaer [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Peter Wostyn, Piet Goddaer ) [22] => Array ( [ArticleId] => 328 [Create_Time] => 2022-06-21 [zipUrl] => https://www.explorationpub.com/uploads/zip/202206/20220628024320.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100423/100423.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100423/100423.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100423/100423_cover.png [JournalsId] => 7 [Title] => The glymphatic system and subarachnoid hemorrhage: disruption and recovery [Abstract] => The glymphatic system, or glial-lymphatic system, is a waste clearance system composed of perivascular channels formed by astrocytes that mediate the clearance of proteins and metabolites from the b [AbstractComplete] =>

The glymphatic system, or glial-lymphatic system, is a waste clearance system composed of perivascular channels formed by astrocytes that mediate the clearance of proteins and metabolites from the brain. These channels facilitate the movement of cerebrospinal fluid throughout brain parenchyma and are critical for homeostasis. Disruption of the glymphatic system leads to an accumulation of these waste products as well as increased interstitial fluid in the brain. These phenomena are also seen during and after subarachnoid hemorrhages (SAH), contributing to the brain damage seen after rupture of a major blood vessel. Herein this review provides an overview of the glymphatic system, its disruption during SAH, and its function in recovery following SAH. The review also outlines drugs which target the glymphatic system and may have therapeutic applications following SAH.

[Names] => Stephan Quintin ... Brandon Lucke-Wold [CName] => [Doi] => 10.37349/ent.2022.00023 [Published] => June 21, 2022 [Viewed] => 2072 [Downloaded] => 76 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00023 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 66 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:118–130 [Recommend] => 0 [Keywords] => Subarachnoid hemorrhage, glymphatic, aquaporin-4, astrocyte, cerebrospinal fluid [DetailTitle] => Emerging Concepts in Subarachnoid Hemorrhage [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/66 [Id] => 100423 [ris] => https://www.explorationpub.com/uploads/Article/A100423/97d9dbeffaab8208b703414a6c420abc.ris [bib] => https://www.explorationpub.com/uploads/Article/A100423/8d883e26e6da834f275c091de3dc1fda.bib [ens] => [Cited] => 5 [Cited_Time] => 2024-05-27 [CitethisArticle] => Quintin S, Barpujari A, Mehkri Y, Hernandez J, Lucke-Wold B. The glymphatic system and subarachnoid hemorrhage: disruption and recovery. Explor Neuroprot Ther. 2022;2:118–30. https://doi.org/10.37349/ent.2022.00023 [Jindex] => 0 [CEmail] => [Ris_Time] => 2022-06-21 06:07:36 [Bib_Time] => 2022-06-21 06:07:36 [KeysWordContens] => The glymphatic system and subarachnoid hemorrhage: disruption and recovery, Subarachnoid hemorrhage, glymphatic, aquaporin-4, astrocyte, cerebrospinal fluid, The glymphatic system, or glial-lymphatic system, is a waste clearance system composed of perivascular channels formed by astrocytes that mediate the clearance of proteins and metabolites from the brain. These channels facilitate the movement of cerebrospinal fluid throughout brain parenchyma and are critical for homeostasis. Disruption of the glymphatic system leads to an accumulation of these waste products as well as increased interstitial fluid in the brain. These phenomena are also seen during and after subarachnoid hemorrhages (SAH), contributing to the brain damage seen after rupture of a major blood vessel. Herein this review provides an overview of the glymphatic system, its disruption during SAH, and its function in recovery following SAH. The review also outlines drugs which target the glymphatic system and may have therapeutic applications following SAH. ,Stephan Quintin ... Brandon Lucke-Wold [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Stephan Quintin, Arnav Barpujari, Yusuf Mehkri, Jairo Hernandez, Brandon Lucke-Wold ) [23] => Array ( [ArticleId] => 342 [Create_Time] => 2022-06-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230804031130.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100424/100424.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100424/100424.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100424/100424_cover.png [JournalsId] => 7 [Title] => Economics of dry needling and botulinum toxin type A for treatment of post-stroke spasticity: a review [Abstract] => Stroke is one of the most common causes of disability and exerts a high burden of direct and indirect costs. Stroke may cause spasticity, which limits patients’ abilities and affects the [AbstractComplete] =>

Stroke is one of the most common causes of disability and exerts a high burden of direct and indirect costs. Stroke may cause spasticity, which limits patients’ abilities and affects their activities of daily living, decreasing their quality of life. Conventional treatments are based on physical therapy, anti-spasticity medication, and botulinum toxin type A (BTX-A). However, recently, non-pharmacological approaches have been used, such as dry needling (DN) of myofascial trigger points. BTX-A and DN are two treatments that aim to decrease spasticity in patients with stroke, but their mode of action, application, and costs differ. Thus, there is a need to determine the comparative economics of post-stroke spasticity treatments. For this purpose, a search for all types of cost-effectiveness studies (randomized controlled trials, matched controls, and cohorts) and models of epidemiological data was performed. Studies were selected if they included economic outcomes in stroke patients treated with BTX-A or DN. As a result, 7 studies of BTX-A and 2 of DN were selected. Similarities were found in the outcomes used to assess the effectiveness of both treatments in most studies, with modifications of the Ashworth Scale [Modified Ashworth Scale (MAS)/Modified Modified Ashworth Scale (MMAS)] and quality-adjusted life year (QALY) being the main indicators of effectiveness. However, both the duration of the studies and the evaluation of costs were highly heterogeneous, making comparison difficult. In conclusion, both BTX-A and DN are cost-effective to treat spasticity in patients with stroke, but there is a need for comparative studies to make direct comparisons of cost-effectiveness with the most frequently used outcomes such as the MMAS and QALYs.

[Names] => Daniel Fernández ... Eva María Gómez-Trullén [CName] => PabloHerrero, [Doi] => 10.37349/ent.2022.00024 [Published] => June 30, 2022 [Viewed] => 1464 [Downloaded] => 65 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00024 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 57 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:131–140 [Recommend] => 0 [Keywords] => Stroke, spasticity, dry needling, botulinum toxin, cost-effectiveness [DetailTitle] => Dry Needling for Neurological Disorders [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/57 [Id] => 100424 [ris] => https://www.explorationpub.com/uploads/Article/A100424/5b76773451106d5776c411c7d20cc9c0.ris [bib] => https://www.explorationpub.com/uploads/Article/A100424/e013e791970e23d34eaf2fa388bb8a15.bib [ens] => [Cited] => 5 [Cited_Time] => 2024-05-27 [CitethisArticle] => Fernández D, Pujol C, Ruber C, Calvo S, Levin MF, Herrero P, et al. Economics of dry needling andbotulinum toxin type A for treatment of post-stroke spasticity: a review. Explor Neuroprot Ther. 2022;2:131-40. https://doi.org/10.37349/ent.2022.00024 [Jindex] => 0 [CEmail] => pherrero@unizar.es, [Ris_Time] => 2023-08-04 03:11:30 [Bib_Time] => 2023-08-04 03:11:30 [KeysWordContens] => Economics of dry needling and botulinum toxin type A for treatment of post-stroke spasticity: a review, Stroke, spasticity, dry needling, botulinum toxin, cost-effectiveness, Stroke is one of the most common causes of disability and exerts a high burden of direct and indirect costs. Stroke may cause spasticity, which limits patients’ abilities and affects their activities of daily living, decreasing their quality of life. Conventional treatments are based on physical therapy, anti-spasticity medication, and botulinum toxin type A (BTX-A). However, recently, non-pharmacological approaches have been used, such as dry needling (DN) of myofascial trigger points. BTX-A and DN are two treatments that aim to decrease spasticity in patients with stroke, but their mode of action, application, and costs differ. Thus, there is a need to determine the comparative economics of post-stroke spasticity treatments. For this purpose, a search for all types of cost-effectiveness studies (randomized controlled trials, matched controls, and cohorts) and models of epidemiological data was performed. Studies were selected if they included economic outcomes in stroke patients treated with BTX-A or DN. As a result, 7 studies of BTX-A and 2 of DN were selected. Similarities were found in the outcomes used to assess the effectiveness of both treatments in most studies, with modifications of the Ashworth Scale [Modified Ashworth Scale (MAS)/Modified Modified Ashworth Scale (MMAS)] and quality-adjusted life year (QALY) being the main indicators of effectiveness. However, both the duration of the studies and the evaluation of costs were highly heterogeneous, making comparison difficult. In conclusion, both BTX-A and DN are cost-effective to treat spasticity in patients with stroke, but there is a need for comparative studies to make direct comparisons of cost-effectiveness with the most frequently used outcomes such as the MMAS and QALYs. ,Daniel Fernández ... Eva María Gómez-Trullén [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Daniel Fernández, Clara Pujol, Carmen Ruber, Sandra Calvo, Mindy F. Levin, Pablo Herrero, Eva María Gómez-Trullén ) [24] => Array ( [ArticleId] => 353 [Create_Time] => 2022-08-11 [zipUrl] => https://www.explorationpub.com/uploads/zip/202208/20220811094721.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100425/100425.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100425/100425.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100425/100425_cover.png [JournalsId] => 7 [Title] => Autism: genetics, environmental stressors, maternal immune activation, and the male bias in autism [Abstract] => Autism spectrum disorder (ASD) is a class of neurodevelopmental disorders (NDD) characterized by deficits in three domains: impairments in social interactions, language, and communication, and increased stereotyped restrictive/repetitive behaviors and interests. The exact etiology of ASD remains unknown. [AbstractComplete] =>

Autism spectrum disorder (ASD) is a class of neurodevelopmental disorders (NDD) characterized by deficits in three domains: impairments in social interactions, language, and communication, and increased stereotyped restrictive/repetitive behaviors and interests. The exact etiology of ASD remains unknown. Genetics, gestational exposure to inflammation, and environmental stressors, which combine to affect mitochondrial dysfunction and metabolism, are implicated yet poorly understood contributors and incompletely delineated pathways toward the relative risk of ASD. Many studies have shown a clear male bias in the incidence of ASD and other NDD. In other words, being male is a significant yet poorly understood risk factor for the development of NDD. This review discusses the link between these factors by looking at the current body of evidence. Understanding the link between the multiplicity of hits—from genes to environmental stressors and possible sexual determinants, contributing to autism susceptibility is critical to developing targeted interventions to mitigate these risks.

[Names] => Sarah Otaru, David A. Lawrence [CName] => [Doi] => 10.37349/ent.2022.00025 [Published] => August 11, 2022 [Viewed] => 1598 [Downloaded] => 47 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00025 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 55 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:141–161 [Recommend] => 0 [Keywords] => Etiology of autism spectrum disorder, mitochondrial dysfunction, oxidative stress, inflammation, gut-brain axis, microbiome [DetailTitle] => Intervention of Neuroimmune Responses [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/55 [Id] => 100425 [ris] => https://www.explorationpub.com/uploads/Article/A100425/f479aa7d881fe2805c0b4af72cc27f1e.ris [bib] => https://www.explorationpub.com/uploads/Article/A100425/3da447c178edd5bf20de46454302e1f8.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Otaru S, Lawrence DA. Autism: genetics, environmental stressors, maternal immune activation, and the male bias in autism. Explor Neuroprot Ther. 2022;2:141–61. https://doi.org/10.37349/ent.2022.00025 [Jindex] => 0 [CEmail] => [Ris_Time] => 2022-08-11 06:58:17 [Bib_Time] => 2022-08-11 06:58:17 [KeysWordContens] => Autism: genetics, environmental stressors, maternal immune activation, and the male bias in autism, Etiology of autism spectrum disorder, mitochondrial dysfunction, oxidative stress, inflammation, gut-brain axis, microbiome, Autism spectrum disorder (ASD) is a class of neurodevelopmental disorders (NDD) characterized by deficits in three domains: impairments in social interactions, language, and communication, and increased stereotyped restrictive/repetitive behaviors and interests. The exact etiology of ASD remains unknown. Genetics, gestational exposure to inflammation, and environmental stressors, which combine to affect mitochondrial dysfunction and metabolism, are implicated yet poorly understood contributors and incompletely delineated pathways toward the relative risk of ASD. Many studies have shown a clear male bias in the incidence of ASD and other NDD. In other words, being male is a significant yet poorly understood risk factor for the development of NDD. This review discusses the link between these factors by looking at the current body of evidence. Understanding the link between the multiplicity of hits—from genes to environmental stressors and possible sexual determinants, contributing to autism susceptibility is critical to developing targeted interventions to mitigate these risks. ,Sarah Otaru, David A. Lawrence [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Sarah Otaru, David A. Lawrence ) [25] => Array ( [ArticleId] => 356 [Create_Time] => 2022-08-23 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230613064952.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100426/100426.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100426/100426.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100426/100426_cover.png [JournalsId] => 7 [Title] => Delayed cerebral ischemia and therapeutic approaches after subarachnoid hemorrhage [Abstract] => Delayed cerebral ischemia after subarachnoid hemorrhage is one of the most important causes of mortality and poor functional outcome in patients. Initially, the etiology and treatment of delayed cer [AbstractComplete] =>

Delayed cerebral ischemia after subarachnoid hemorrhage is one of the most important causes of mortality and poor functional outcome in patients. Initially, the etiology and treatment of delayed cerebral ischemia focused primarily on cerebral vasospasm. However, recent studies have detected that depolarization, microcirculation, and autoregulation disorder, which spreads together with cerebral vasospasm, also play a role in the etiology. The main treatment strategies in the prevention and treatment of delayed cerebral ischemia are the regulation of blood pressure and the use of calcium channel blockers, especially nimodipine. The main step in the early diagnosis and treatment of the disease is to monitor the neurological clinical status. In addition to transcranial Doppler ultrasonography, computed tomography, or magnetic resonance imaging angiography, continuous electroencephalography and invasive brain multimodal examination may be required in the follow-up period of the disease. In addition to blood pressure regulation, optimization of cardiac output, endovascular interventions, angioplasty, and/or intra-arterial vasodilator infusion are other treatment methods. This review aimed to evaluate delayed cerebral ischemia, one of the most important complications of subarachnoid hemorrhage, in the light of current literature.

[Names] => Fettah Eren ... Sueda Ecem Yilmaz [CName] => FettahEren, [Doi] => 10.37349/ent.2022.00026 [Published] => August 22, 2022 [Viewed] => 1379 [Downloaded] => 59 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00026 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 66 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:162–173 [Recommend] => 0 [Keywords] => Subarachnoid hemorrhage, delayed cerebral ischemia, treatment approaches, nimodipine [DetailTitle] => Emerging Concepts in Subarachnoid Hemorrhage [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/66 [Id] => 100426 [ris] => https://www.explorationpub.com/uploads/Article/A100426/19d59ef14e214c22e5ec3a803a346a9c.ris [bib] => https://www.explorationpub.com/uploads/Article/A100426/e61e9ec0ac3c583498e102ff5b9c25c7.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Eren F, Yildogan AT, Demir A, Ozguncu C, Yilmaz SE. Delayed cerebral ischemia and therapeutic approaches after subarachnoid hemorrhage. Explor Neuroprot Ther. 2022;2:162–73. https://doi.org/10.37349/ent.2022.00026 [Jindex] => 0 [CEmail] => dreren42@hotmail.com, [Ris_Time] => 2022-08-22 09:49:33 [Bib_Time] => 2022-08-22 09:49:33 [KeysWordContens] => Delayed cerebral ischemia and therapeutic approaches after subarachnoid hemorrhage, Subarachnoid hemorrhage, delayed cerebral ischemia, treatment approaches, nimodipine, Delayed cerebral ischemia after subarachnoid hemorrhage is one of the most important causes of mortality and poor functional outcome in patients. Initially, the etiology and treatment of delayed cerebral ischemia focused primarily on cerebral vasospasm. However, recent studies have detected that depolarization, microcirculation, and autoregulation disorder, which spreads together with cerebral vasospasm, also play a role in the etiology. The main treatment strategies in the prevention and treatment of delayed cerebral ischemia are the regulation of blood pressure and the use of calcium channel blockers, especially nimodipine. The main step in the early diagnosis and treatment of the disease is to monitor the neurological clinical status. In addition to transcranial Doppler ultrasonography, computed tomography, or magnetic resonance imaging angiography, continuous electroencephalography and invasive brain multimodal examination may be required in the follow-up period of the disease. In addition to blood pressure regulation, optimization of cardiac output, endovascular interventions, angioplasty, and/or intra-arterial vasodilator infusion are other treatment methods. This review aimed to evaluate delayed cerebral ischemia, one of the most important complications of subarachnoid hemorrhage, in the light of current literature. ,Fettah Eren ... Sueda Ecem Yilmaz [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Fettah Eren, Aydin Talip Yildogan, Aysegul Demir, Cihat Ozguncu, Sueda Ecem Yilmaz ) [26] => Array ( [ArticleId] => 381 [Create_Time] => 2022-08-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230613060140.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100427/100427.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100427/100427.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100427/100427_cover.png [JournalsId] => 7 [Title] => Paraclinoid unruptured giant aneurysm with therapeutic success [Abstract] => The global prevalence of intracranial aneurysms (IA) ranges from 5–10%, with a demographic variation. Large and giant aneurysms typically involve cavernous and paraclinoid se [AbstractComplete] =>

The global prevalence of intracranial aneurysms (IA) ranges from 5–10%, with a demographic variation. Large and giant aneurysms typically involve cavernous and paraclinoid segments of the internal carotid artery (ICA), and represent 5% of IA. Typically, these lesions involve segments of the ICA, especially the cavernous and paraclinoid segments. The remaining cases affect the vertebrobasilar region, middle cerebral artery (MCA), and anterior cerebral artery (ACA). From the morphological point of view, they are divided into saccular and fusiform. In cases of rupture, the subarachnoid hemorrhage (SAH) is the most common presentation followed by intracerebral hemorrhage (ICH), or both. Other manifestations can occur as occlusion of perforating vessels, embolic events, seizures, and mass effects. The management of unruptured intracranial aneurysms (UIA) is controversial, and the aim of treatment is to exclude the lesions and preserve neurological function. Endovascular techniques for the treatment of paraclinoid aneurysms, in particular, ICA reconstruction using flow-diverting stents, have become a valid option. However, surgery or endovascular treatment has a number of limitations and the choice of treatment is individual in each case. This type of lesion has an extremely poor natural history, and treatment is a challenge regardless of the technique used.

The report described a clinical case of a 55-year-old female, with a personal history of hypertension, hyperthyroidism, and depressive syndrome. The patient started complaints of moderate-intensity right frontal headache, progressively worsening with two months of evolution. She also reported blurred vision and diplopia. Brain computed tomography (CT) documented a partially calcified sellar and parasellar lesion. Subsequently, magnetic resonance imaging (MRI)/MRI angiographies were performed and showed a saccular aneurysm of the right ICA, cavernous segment. The patient underwent a diagnostic and therapeutic angiography with stent placement. Clinical and imaging improvements were documented by angiography and MRI angiography with progressive reduction of the aneurysm during the period of follow-up.

[Names] => Gonçalo Januário [CName] => GonçaloJanuário, [Doi] => 10.37349/ent.2022.00027 [Published] => August 30, 2022 [Viewed] => 1435 [Downloaded] => 37 [Subject] => Case Report [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00027 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 66 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:174–181 [Recommend] => 0 [Keywords] => Giant aneurysm, unruptured, paraclinoid internal carotid artery, embolization, flow diverter device [DetailTitle] => Emerging Concepts in Subarachnoid Hemorrhage [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/66 [Id] => 100427 [ris] => https://www.explorationpub.com/uploads/Article/A100427/0f89223f0188f546061203a9f525c1e6.ris [bib] => https://www.explorationpub.com/uploads/Article/A100427/edfadefce240d5a887e63ada5f58b8a5.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Gonçalo J. Paraclinoid unruptured giant aneurysm with therapeutic success. Explor Neuroprot Ther. 2022;2:174–81. https://doi.org/10.37349/ent.2022.00027 [Jindex] => 0 [CEmail] => jg.machado@hotmail.com, [Ris_Time] => 2022-08-30 01:11:11 [Bib_Time] => 2022-08-30 01:11:11 [KeysWordContens] => Paraclinoid unruptured giant aneurysm with therapeutic success, Giant aneurysm, unruptured, paraclinoid internal carotid artery, embolization, flow diverter device, The global prevalence of intracranial aneurysms (IA) ranges from 5–10%, with a demographic variation. Large and giant aneurysms typically involve cavernous and paraclinoid segments of the internal carotid artery (ICA), and represent 5% of IA. Typically, these lesions involve segments of the ICA, especially the cavernous and paraclinoid segments. The remaining cases affect the vertebrobasilar region, middle cerebral artery (MCA), and anterior cerebral artery (ACA). From the morphological point of view, they are divided into saccular and fusiform. In cases of rupture, the subarachnoid hemorrhage (SAH) is the most common presentation followed by intracerebral hemorrhage (ICH), or both. Other manifestations can occur as occlusion of perforating vessels, embolic events, seizures, and mass effects. The management of unruptured intracranial aneurysms (UIA) is controversial, and the aim of treatment is to exclude the lesions and preserve neurological function. Endovascular techniques for the treatment of paraclinoid aneurysms, in particular, ICA reconstruction using flow-diverting stents, have become a valid option. However, surgery or endovascular treatment has a number of limitations and the choice of treatment is individual in each case. This type of lesion has an extremely poor natural history, and treatment is a challenge regardless of the technique used. The report described a clinical case of a 55-year-old female, with a personal history of hypertension, hyperthyroidism, and depressive syndrome. The patient started complaints of moderate-intensity right frontal headache, progressively worsening with two months of evolution. She also reported blurred vision and diplopia. Brain computed tomography (CT) documented a partially calcified sellar and parasellar lesion. Subsequently, magnetic resonance imaging (MRI)/MRI angiographies were performed and showed a saccular aneurysm of the right ICA, cavernous segment. The patient underwent a diagnostic and therapeutic angiography with stent placement. Clinical and imaging improvements were documented by angiography and MRI angiography with progressive reduction of the aneurysm during the period of follow-up. ,Gonçalo Januário [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Gonçalo Januário ) [27] => Array ( [ArticleId] => 422 [Create_Time] => 2022-10-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202211/20221115070938.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100428/100428.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100428/100428.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100428/100428_cover.png [JournalsId] => 7 [Title] => Toll-like receptor 4 in the interface between neuroimmune response and behavioral alterations caused by stress [Abstract] => Different stressors can elicit neuroinflammatory responses modulated by innate immunity receptors, such as the family of Toll-like receptors (TLRs). The TLR4, a pattern recognition receptor (PRR), i [AbstractComplete] =>

Different stressors can elicit neuroinflammatory responses modulated by innate immunity receptors, such as the family of Toll-like receptors (TLRs). The TLR4, a pattern recognition receptor (PRR), is involved in many diseases, such as inflammatory and central nervous system (CNS) diseases. Stress exposure can regulate the expression of PRRs, including TLR4, in the brain of animals, especially in the hippocampus and prefrontal cortex. Moreover, TLR4 modulates behavior and neuroinflammatory responses in the brain. In addition, to TLR4, the endocannabinoid (eCB) system plays a role in stress response and immunity, acting as a regulatory, stress-buffer system. This system is involved in many TLRs-mediated immune responses, such as microglia activation. Therefore, pharmacological approaches targeting the eCB system could modulate neuroinflammatory responses to stress by interfering with the TLR4 pathway. Although the connection between TLR4, stress, and neuroinflammation is well documented, almost no pre-clinical studies investigate the possible direct relationship between TLR4, behavior, stress, and the eCB system. Studies exploring the relationship between stress, neuroinflammation, TLR4, and the eCB system were searched using Pubmed, Web of Science, and Embase databases. Based on this search, this review is focused on the involvement of TLR4 receptors and signaling in neuroinflammation and the behavioral consequences of stress exposure. Moreover, evidence of the eCB system modulating TLR4-mediated responses was brought to the attention, pointing out a possible regulatory role of these responses by eCBs in behavior changes related to mood disorders.

[Names] => Fábio José Coelho Souza-Junior ... Sabrina Francesca Lisboa [CName] => Sabrina FrancescaLisboa, [Doi] => 10.37349/ent.2022.00028 [Published] => October 31, 2022 [Viewed] => 2042 [Downloaded] => 73 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00028 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 55 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:182–209 [Recommend] => 0 [Keywords] => Stress, Toll-like receptor 4, microglia, behavior, endocannabinoid system [DetailTitle] => Intervention of Neuroimmune Responses [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/55 [Id] => 100428 [ris] => https://www.explorationpub.com/uploads/Article/A100428/b1b1b55b8d39d9dac14495d590bd09b8.ris [bib] => https://www.explorationpub.com/uploads/Article/A100428/b9de36b3ee68a932a0dc7c8105cc1e4b.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-05-27 [CitethisArticle] => Souza-Junior FJC, Cunha LC, Lisboa SF. Toll-like receptor 4 in the interface between neuroimmune response and behavioral alterations caused by stress. Explor Neuroprot Ther. 2022;2:182–209. https://doi.org/10.37349/ent.2022.00028 [Jindex] => 0 [CEmail] => sabrinalisboa@usp.br, [Ris_Time] => 2022-10-28 11:16:25 [Bib_Time] => 2022-10-31 12:34:55 [KeysWordContens] => Toll-like receptor 4 in the interface between neuroimmune response and behavioral alterations caused by stress, Stress, Toll-like receptor 4, microglia, behavior, endocannabinoid system, Different stressors can elicit neuroinflammatory responses modulated by innate immunity receptors, such as the family of Toll-like receptors (TLRs). The TLR4, a pattern recognition receptor (PRR), is involved in many diseases, such as inflammatory and central nervous system (CNS) diseases. Stress exposure can regulate the expression of PRRs, including TLR4, in the brain of animals, especially in the hippocampus and prefrontal cortex. Moreover, TLR4 modulates behavior and neuroinflammatory responses in the brain. In addition, to TLR4, the endocannabinoid (eCB) system plays a role in stress response and immunity, acting as a regulatory, stress-buffer system. This system is involved in many TLRs-mediated immune responses, such as microglia activation. Therefore, pharmacological approaches targeting the eCB system could modulate neuroinflammatory responses to stress by interfering with the TLR4 pathway. Although the connection between TLR4, stress, and neuroinflammation is well documented, almost no pre-clinical studies investigate the possible direct relationship between TLR4, behavior, stress, and the eCB system. Studies exploring the relationship between stress, neuroinflammation, TLR4, and the eCB system were searched using Pubmed, Web of Science, and Embase databases. Based on this search, this review is focused on the involvement of TLR4 receptors and signaling in neuroinflammation and the behavioral consequences of stress exposure. Moreover, evidence of the eCB system modulating TLR4-mediated responses was brought to the attention, pointing out a possible regulatory role of these responses by eCBs in behavior changes related to mood disorders. ,Fábio José Coelho Souza-Junior ... Sabrina Francesca Lisboa [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Fábio José Coelho Souza-Junior, Laura Colete Cunha, Sabrina Francesca Lisboa ) [28] => Array ( [ArticleId] => 431 [Create_Time] => 2022-11-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202210/20221031073018.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100429/100429.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100429/100429.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100429/100429_cover.png [JournalsId] => 7 [Title] => Overview of biomarkers in myasthenia gravis [Abstract] => Myasthenia gravis (MG) is a rare auto-immune neuromuscular junction (NMJ) disorder which is caused by formation of autoantibodies and destruction of NMJ components. The MG diagnosis is based on the [AbstractComplete] =>

Myasthenia gravis (MG) is a rare auto-immune neuromuscular junction (NMJ) disorder which is caused by formation of autoantibodies and destruction of NMJ components. The MG diagnosis is based on the symptoms, autoantibodies detection and paraclinical tests. Given that MG patients have so many differential diagnosis and various medication responses, choosing an accurate diagnosis and the therapy plan in MG is challenging. According to the studies, there are the immunologic, genetic, microRNAs, gut microbiome, and other established or newly proposed biomarkers for diagnosis and prognosis of MG. More studies are needed to provide better collection of biomarkers in MG patients and evaluate their role in MG pathology.

[Names] => Fatemeh Afrashteh, Rayan Rajabi [CName] => [Doi] => 10.37349/ent.2022.00029 [Published] => October 31, 2022 [Viewed] => 1717 [Downloaded] => 77 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00029 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 79 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:210–225 [Recommend] => 0 [Keywords] => Myasthenia gravis, biomarker, autoimmune disease, neuromuscular junction [DetailTitle] => The Future of Biomarkers in CNS Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/79 [Id] => 100429 [ris] => https://www.explorationpub.com/uploads/Article/A100429/ca3b63c904a97d74d1901f269c255afc.ris [bib] => https://www.explorationpub.com/uploads/Article/A100429/e4ad56fd83c7207b0c9eb1f241573765.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Afrashteh F, Rajabi R. Overview of biomarkers in myasthenia gravis. Explor Neuroprot Ther. 2022;2:210–25. https://doi.org/10.37349/ent.2022.00029 [Jindex] => 0 [CEmail] => [Ris_Time] => 2022-10-31 07:30:44 [Bib_Time] => 2022-10-31 07:30:44 [KeysWordContens] => Overview of biomarkers in myasthenia gravis, Myasthenia gravis, biomarker, autoimmune disease, neuromuscular junction, Myasthenia gravis (MG) is a rare auto-immune neuromuscular junction (NMJ) disorder which is caused by formation of autoantibodies and destruction of NMJ components. The MG diagnosis is based on the symptoms, autoantibodies detection and paraclinical tests. Given that MG patients have so many differential diagnosis and various medication responses, choosing an accurate diagnosis and the therapy plan in MG is challenging. According to the studies, there are the immunologic, genetic, microRNAs, gut microbiome, and other established or newly proposed biomarkers for diagnosis and prognosis of MG. More studies are needed to provide better collection of biomarkers in MG patients and evaluate their role in MG pathology. ,Fatemeh Afrashteh, Rayan Rajabi [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Fatemeh Afrashteh, Rayan Rajabi ) [29] => Array ( [ArticleId] => 433 [Create_Time] => 2022-11-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202211/20221101011629.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100430/100430.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100430/100430.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100430/100430_cover.png [JournalsId] => 7 [Title] => Blockage of thrombospondin 4 secreted by spinal astrocytes may be a promising therapeutic target in the treatment of neuropathic pain [Abstract] => Neuropathic pain (NP), which is difficult to treat, remains a heavy burden for both individuals and society. The efficacy of current treatments is insufficient. The pathophysiology of NP is still no [AbstractComplete] =>

Neuropathic pain (NP), which is difficult to treat, remains a heavy burden for both individuals and society. The efficacy of current treatments is insufficient. The pathophysiology of NP is still not fully elucidated, and there is a need to explore new therapeutic targets to develop more effective treatment strategies. Recent studies showed that thrombospondin 4 (TSP4) protein expression is increased in the spinal cord following nervous system injury and that blocking or inhibiting this increase improves NP. In this review, it has been aimed to present the evidence for the role of TSP4 in the mechanisms of NP development and to evaluate the therapeutic potential of TSP4 blockade in the treatment of NP.

The relationship between TSP4 protein level in the spinal cord and behavioral hypersensitivity in rodents. This illustration has been created to collectively reflect the results of experimental animal studies investigating the relationship between the TSP4 levels in the spinal cord and NP. For more detailed information on related studies, please see the “Evidence of the relationship between TSP4 and NP” section of the article and tables

[Names] => Neslihan Düzenli ... Aytül Önal [CName] => [Doi] => 10.37349/ent.2022.00030 [Published] => October 31, 2022 [Viewed] => 1341 [Downloaded] => 45 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00030 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 74 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:226–241 [Recommend] => 0 [Keywords] => Astrocyte, dorsal root ganglion, neuropathic pain, nerve injury, rodent, spinal cord, thrombospondin 4 [DetailTitle] => Glia and Neuroprotection [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/74 [Id] => 100430 [ris] => https://www.explorationpub.com/uploads/Article/A100430/2bda9a9e88621271b61fdcbd90b027a3.ris [bib] => https://www.explorationpub.com/uploads/Article/A100430/50589189aeb107da1d2322a847bfd39a.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Düzenli N, Can C, Önal A. Blockage of thrombospondin 4 secreted by spinal astrocytes may be a promising therapeutic target in the treatment of neuropathic pain. Explor Neuroprot Ther. 2022;2:226–41. https://doi.org/10.37349/ent.2022.00030 [Jindex] => 0 [CEmail] => [Ris_Time] => 2022-10-31 07:25:15 [Bib_Time] => 2022-10-31 07:25:15 [KeysWordContens] => Blockage of thrombospondin 4 secreted by spinal astrocytes may be a promising therapeutic target in the treatment of neuropathic pain, Astrocyte, dorsal root ganglion, neuropathic pain, nerve injury, rodent, spinal cord, thrombospondin 4, Neuropathic pain (NP), which is difficult to treat, remains a heavy burden for both individuals and society. The efficacy of current treatments is insufficient. The pathophysiology of NP is still not fully elucidated, and there is a need to explore new therapeutic targets to develop more effective treatment strategies. Recent studies showed that thrombospondin 4 (TSP4) protein expression is increased in the spinal cord following nervous system injury and that blocking or inhibiting this increase improves NP. In this review, it has been aimed to present the evidence for the role of TSP4 in the mechanisms of NP development and to evaluate the therapeutic potential of TSP4 blockade in the treatment of NP. Graphical abstract.The relationship between TSP4 protein level in the spinal cord and behavioral hypersensitivity in rodents. This illustration has been created to collectively reflect the results of experimental animal studies investigating the relationship between the TSP4 levels in the spinal cord and NP. For more detailed information on related studies, please see the “Evidence of the relationship between TSP4 and NP” section of the article and tables ,Neslihan Düzenli ... Aytül Önal [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 [AuthorsName] => Neslihan Düzenli, Cenk Can, Aytül Önal ) [30] => Array ( [ArticleId] => 435 [Create_Time] => 2022-11-16 [zipUrl] => https://www.explorationpub.com/uploads/zip/202212/20221229030145.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100431/100431.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100431/100431.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100431/100431_cover.png [JournalsId] => 7 [Title] => Dry needling with electrical stimulation for the treatment of a pediatric patient with spastic cerebral palsy: a case report [Abstract] => The patient was a 6-year-old child with spastic quadriplegic cerebral palsy (CP) categorized with the gross motor function classification system (GMFCS) as a level IV and a Modified Modified Ashwort [AbstractComplete] =>

The patient was a 6-year-old child with spastic quadriplegic cerebral palsy (CP) categorized with the gross motor function classification system (GMFCS) as a level IV and a Modified Modified Ashworth Scale (MMAS) of 2 for the bilateral hamstring and hip adductor muscles, and 3 for the bilateral gastrocnemius muscles. This patient’s limited range of motion significantly affected the caregiver’s ability to perform activities of daily living (ADLs). Dry needling (DN) is considered a standard treatment (TX) when treating adults with poor range of motion. This article aims to place intramuscular electrical stimulation (IMES), the delivery of an electrical current through a monofilament needle into targeted trigger points (TrPs) within the context of treating children with spastic CP. Following IMES TXs over 32 months that totaled 12 left hamstring TXs, 13 right hamstring TXs, 13 hip adductor TXs, 21 left gastrocnemius TXs, and 18 right gastrocnemius TXs, the patient demonstrated an increase in passive range of motion (PROM) of the hamstring, hip adductors, and gastrocnemius muscles. These gains equated to ease in ADLs. Both the Pediatric Evaluation of Disability Inventory (PEDI, PEDI-Caregiver Assistance Scale) and the Goal Attainment Scale (GAS) demonstrated decreased caregiver burden. The child’s GMFCS level and the MMAS did not change. Further data collection related to treating children with spasticity using IMES is indicated to validate this type of TX with this patient population.

[Names] => Temrah Okonski, Jan Dommerholt [CName] => [Doi] => 10.37349/ent.2022.00031 [Published] => November 16, 2022 [Viewed] => 1344 [Downloaded] => 55 [Subject] => Case Report [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00031 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 57 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:242–255 [Recommend] => 0 [Keywords] => Spasticity, cerebral palsy, dry needling, electrical stimulation, case report [DetailTitle] => Dry Needling for Neurological Disorders [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/57 [Id] => 100431 [ris] => https://www.explorationpub.com/uploads/Article/A100431/927b61e33e0ffd3317c623820791e2a3.ris [bib] => https://www.explorationpub.com/uploads/Article/A100431/0ba8d752d527421288ee44c0d53d2326.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-05-25 [CitethisArticle] => Okonski T, Dommerholt J. Dry needling with electrical stimulation for the treatment of a pediatric patient with spastic cerebral palsy: a case report. Explor Neuroprot Ther. 2022;2:242–55. https://doi.org/10.37349/ent.2022.00031 [Jindex] => 0 [CEmail] => [Ris_Time] => 2022-11-15 07:44:28 [Bib_Time] => 2022-11-15 07:44:28 [KeysWordContens] => Dry needling with electrical stimulation for the treatment of a pediatric patient with spastic cerebral palsy: a case report, Spasticity, cerebral palsy, dry needling, electrical stimulation, case report, The patient was a 6-year-old child with spastic quadriplegic cerebral palsy (CP) categorized with the gross motor function classification system (GMFCS) as a level IV and a Modified Modified Ashworth Scale (MMAS) of 2 for the bilateral hamstring and hip adductor muscles, and 3 for the bilateral gastrocnemius muscles. This patient’s limited range of motion significantly affected the caregiver’s ability to perform activities of daily living (ADLs). Dry needling (DN) is considered a standard treatment (TX) when treating adults with poor range of motion. This article aims to place intramuscular electrical stimulation (IMES), the delivery of an electrical current through a monofilament needle into targeted trigger points (TrPs) within the context of treating children with spastic CP. Following IMES TXs over 32 months that totaled 12 left hamstring TXs, 13 right hamstring TXs, 13 hip adductor TXs, 21 left gastrocnemius TXs, and 18 right gastrocnemius TXs, the patient demonstrated an increase in passive range of motion (PROM) of the hamstring, hip adductors, and gastrocnemius muscles. These gains equated to ease in ADLs. Both the Pediatric Evaluation of Disability Inventory (PEDI, PEDI-Caregiver Assistance Scale) and the Goal Attainment Scale (GAS) demonstrated decreased caregiver burden. The child’s GMFCS level and the MMAS did not change. Further data collection related to treating children with spasticity using IMES is indicated to validate this type of TX with this patient population. ,Temrah Okonski, Jan Dommerholt [PublishedText] => Published [IsEdit] => 0 [AccountId] => 46 [Zh] => 1 [AuthorsName] => Temrah Okonski, Jan Dommerholt ) [31] => Array ( [ArticleId] => 450 [Create_Time] => 2022-12-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230613055327.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100432/100432.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100432/100432.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100432/100424_cover.png [JournalsId] => 7 [Title] => Catatonia in two women with Parkinson’s disease treated with electroconvulsive therapy [Abstract] => Catatonia is a neuropsychiatric syndrome characterized by a broad range of motor, behavioral and cognitive abnormalities. Catatonia and Parkinson’s disease (PD) may show partially overlapping symptomatology. For this reason, catatonia could be misdiagnosed and overlooked in patients with severe PD, leading to a delay in proper treatment with benzodiazepines or electroconvulsive therapy (ECT). [AbstractComplete] =>

Catatonia is a neuropsychiatric syndrome characterized by a broad range of motor, behavioral and cognitive abnormalities. Catatonia and Parkinson’s disease (PD) may show partially overlapping symptomatology. For this reason, catatonia could be misdiagnosed and overlooked in patients with severe PD, leading to a delay in proper treatment with benzodiazepines or electroconvulsive therapy (ECT). Two cases of women with PD and catatonia who have been admitted and treated with ECT at the University Hospital of Pisa are described here. Both had a history of bipolar disorder and developed withdrawn catatonia, in the context of affective episodes, approximately one year after the diagnosis of PD. In both cases, ECT was needed and successfully led to the remission of catatonic symptoms, without cognitive worsening. Since ECT appears to effectively treat catatonia in patients with PD, clinicians should consider it as a therapeutic option.

[Names] => Camilla Elefante ... Giulio Perugi [CName] => CamillaElefante, [Doi] => 10.37349/ent.2022.00032 [Published] => December 28, 2022 [Viewed] => 1594 [Downloaded] => 36 [Subject] => Case Report [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00032 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:256–263 [Recommend] => 0 [Keywords] => Catatonia, Parkinson’s disease, electroconvulsive therapy, mood disorder, movement disorders [DetailTitle] => [DetailUrl] => [Id] => 100432 [ris] => https://www.explorationpub.com/uploads/Article/A100432/59adf5ba75c7a023505a92cb76164e25.ris [bib] => https://www.explorationpub.com/uploads/Article/A100432/3b04ffdb7af2b5aa5832a4a99b9f33e4.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Elefante C, Brancati GE, Tripodi B, Torrigiani S, Lattanzi L, Medda P, et al. Catatonia in two women with Parkinson’s disease treated with electroconvulsive therapy. Explor Neuroprot Ther. 2022;2:256–63. https://doi.org/10.37349/ent.2022.00032 [Jindex] => 0 [CEmail] => camilla.elefante@phd.unipi.it, [Ris_Time] => 2022-12-28 02:58:00 [Bib_Time] => 2022-12-28 02:58:00 [KeysWordContens] => Catatonia in two women with Parkinson’s disease treated with electroconvulsive therapy, Catatonia, Parkinson’s disease, electroconvulsive therapy, mood disorder, movement disorders, Catatonia is a neuropsychiatric syndrome characterized by a broad range of motor, behavioral and cognitive abnormalities. Catatonia and Parkinson’s disease (PD) may show partially overlapping symptomatology. For this reason, catatonia could be misdiagnosed and overlooked in patients with severe PD, leading to a delay in proper treatment with benzodiazepines or electroconvulsive therapy (ECT). Two cases of women with PD and catatonia who have been admitted and treated with ECT at the University Hospital of Pisa are described here. Both had a history of bipolar disorder and developed withdrawn catatonia, in the context of affective episodes, approximately one year after the diagnosis of PD. In both cases, ECT was needed and successfully led to the remission of catatonic symptoms, without cognitive worsening. Since ECT appears to effectively treat catatonia in patients with PD, clinicians should consider it as a therapeutic option. ,Camilla Elefante ... Giulio Perugi [PublishedText] => Published [IsEdit] => 0 [AccountId] => 24 [Zh] => 1 [AuthorsName] => Camilla Elefante, Giulio E. Brancati, Beniamino Tripodi, Samuele Torrigiani, Lorenzo Lattanzi, Pierpaolo Medda, Giulio Perugi ) [32] => Array ( [ArticleId] => 460 [Create_Time] => 2022-12-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202212/20221230072405.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100433/100433.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100433/100433.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100433/100433_cover.png [JournalsId] => 7 [Title] => Biomarkers in small fiber neuropathy [Abstract] => Small fiber neuropathy (SFN) is a relatively common, but largely understudied neurological syndrome which has affected the lives of many globally. The common symptoms of SFN include pain, dysesthesi [AbstractComplete] =>

Small fiber neuropathy (SFN) is a relatively common, but largely understudied neurological syndrome which has affected the lives of many globally. The common symptoms of SFN include pain, dysesthesia, and autonomic dysfunction, which are caused by damage to small nerve fibers. Due to its heterogeneous nature, SFN causes a multitude of symptoms which makes the disease and its subtypes difficult to diagnose. Furthermore, as the pathophysiology of SFN remains largely enigmatic, no cause is found in around 50% of the cases and these are classified as idiopathic SFN (iSFN). The difficult task of diagnosing SFN, and the even more elusive feat of hunting for the underlying etiology, demands accurate, precise, preferably noninvasive, and affordable tools, or a combination of them. Accordingly, appropriate biomarkers for SFN are needed to stratify patients and develop cause-centered treatments in addition to symptomatic treatments. As peripheral axons grow and repair, identifying underlying causes of SFN and intervening early may spur axonal regeneration in young patients, which can greatly improve their symptoms and improve quality of life. This narrative review aims to objectively highlight functional, histological, and molecular biomarkers to aid clinicians in discerning the diagnostic tests they should use to diagnose, confirm and determine the etiology of SFN. The strengths and limitations of each potential biomarker will be discussed. Clearer diagnostic criteria, guidelines, and work-up for SFN are required for clinicians to better identify the disease in patients presenting with non-specific symptoms.

[Names] => Amanda C. Y. Chan ... Joy Vijayan [CName] => [Doi] => 10.37349/ent.2022.00033 [Published] => December 30, 2022 [Viewed] => 2940 [Downloaded] => 67 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2022.00033 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 79 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2022;2:264–283 [Recommend] => 0 [Keywords] => Small fiber neuropathy, biomarkers, antibodies, skin biopsy, intra-epidermal nerve fiber density [DetailTitle] => The Future of Biomarkers in CNS Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/79 [Id] => 100433 [ris] => https://www.explorationpub.com/uploads/Article/A100433/bbec64275055540ce09324ed65557050.ris [bib] => https://www.explorationpub.com/uploads/Article/A100433/f21783aafbda69e81e280e31fe0fe725.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Chan ACY, Ong K, Ong JJY, Sharma VK, Wong HY, Vijayan J. Biomarkers in small fiber neuropathy. Explor Neuroprot Ther. 2022;2:264–83. https://doi.org/10.37349/ent.2022.00033 [Jindex] => 0 [CEmail] => [Ris_Time] => 2022-12-29 02:48:33 [Bib_Time] => 2022-12-29 02:48:33 [KeysWordContens] => Biomarkers in small fiber neuropathy, Small fiber neuropathy, biomarkers, antibodies, skin biopsy, intra-epidermal nerve fiber density, Small fiber neuropathy (SFN) is a relatively common, but largely understudied neurological syndrome which has affected the lives of many globally. The common symptoms of SFN include pain, dysesthesia, and autonomic dysfunction, which are caused by damage to small nerve fibers. Due to its heterogeneous nature, SFN causes a multitude of symptoms which makes the disease and its subtypes difficult to diagnose. Furthermore, as the pathophysiology of SFN remains largely enigmatic, no cause is found in around 50% of the cases and these are classified as idiopathic SFN (iSFN). The difficult task of diagnosing SFN, and the even more elusive feat of hunting for the underlying etiology, demands accurate, precise, preferably noninvasive, and affordable tools, or a combination of them. Accordingly, appropriate biomarkers for SFN are needed to stratify patients and develop cause-centered treatments in addition to symptomatic treatments. As peripheral axons grow and repair, identifying underlying causes of SFN and intervening early may spur axonal regeneration in young patients, which can greatly improve their symptoms and improve quality of life. This narrative review aims to objectively highlight functional, histological, and molecular biomarkers to aid clinicians in discerning the diagnostic tests they should use to diagnose, confirm and determine the etiology of SFN. The strengths and limitations of each potential biomarker will be discussed. Clearer diagnostic criteria, guidelines, and work-up for SFN are required for clinicians to better identify the disease in patients presenting with non-specific symptoms. ,Amanda C. Y. Chan ... Joy Vijayan [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 [AuthorsName] => Amanda C. Y. Chan, Kathleen Ong, Jonathan J. Y. Ong, Vijay K. Sharma, Hiu Yi Wong, Joy Vijayan ) [33] => Array ( [ArticleId] => 472 [Create_Time] => 2023-02-21 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240407081249.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100434/100434.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100434/100434.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100434/100434_cover.png [JournalsId] => 7 [Title] => Machine learning as a new tool in neurological disease prevention, diagnosis, and treatment [Abstract] => More than 600 different neurological diseases affect the human population. Some of these are genetic and can emerge even before birth, and some are caused by defects, infections, trauma, degeneratio [AbstractComplete] =>

More than 600 different neurological diseases affect the human population. Some of these are genetic and can emerge even before birth, and some are caused by defects, infections, trauma, degeneration, inflammation, and cancer. However, they all share disabilities caused by damage to the nervous system. In the last decades, the burden of almost all neurological disorders has increased in terms of absolute incidence, prevalence, and mortality, largely due to the population’s growth and aging. This represents a dangerous trend and should become our priority for the future. But what new goals are we going to set and reach now, and how will we exploit thought-provoking technological skills for making these goals feasible? Machine learning can be at the root of the problem. Indeed, most recently, there has been a push towards medical data analysis by machine learning, and a great improvement in the training capabilities particularly of artificial deep neural networks (DNNs) inspired by the biological neural networks characterizing the human brain. This has generated competitive results for applications such as biomolecular target and protein structure prediction, structure-based rational drug design, and repurposing, all exerting a major impact on neuroscience and human well-being. By approaching early risks for diseases, non-invasive diagnosis, personalized treatment assessment, drug discovery, and automated science, the machine learning arena has thus the potential of becoming the new frontier for empowering neuroscience research and clinical practice in the years ahead.

[Names] => Cinzia Volonté [CName] => CinziaVolonté, [Doi] => 10.37349/ent.2023.00034 [Published] => February 21, 2023 [Viewed] => 1031 [Downloaded] => 35 [Subject] => Perspective [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00034 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:1–7 [Recommend] => 0 [Keywords] => Machine learning, neural networks, neurological diseases [DetailTitle] => [DetailUrl] => [Id] => 100434 [ris] => https://www.explorationpub.com/uploads/Article/A100434/9b5a91c987bd15da961d19b30166a1cd.ris [bib] => https://www.explorationpub.com/uploads/Article/A100434/07652c424ca5860c8dcf94d9002e2737.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Volonté C. Machine learning as a new tool in neurological disease prevention, diagnosis, and treatment. Explor Neuroprot Ther. 2023;3:1–7. https://doi.org/10.37349/ent.2023.00034 [Jindex] => 0 [CEmail] => cinzia.volonte@cnr.it, [Ris_Time] => 2023-02-21 01:04:54 [Bib_Time] => 2023-02-21 01:04:54 [KeysWordContens] => Machine learning as a new tool in neurological disease prevention, diagnosis, and treatment, Machine learning, neural networks, neurological diseases, More than 600 different neurological diseases affect the human population. Some of these are genetic and can emerge even before birth, and some are caused by defects, infections, trauma, degeneration, inflammation, and cancer. However, they all share disabilities caused by damage to the nervous system. In the last decades, the burden of almost all neurological disorders has increased in terms of absolute incidence, prevalence, and mortality, largely due to the population’s growth and aging. This represents a dangerous trend and should become our priority for the future. But what new goals are we going to set and reach now, and how will we exploit thought-provoking technological skills for making these goals feasible? Machine learning can be at the root of the problem. Indeed, most recently, there has been a push towards medical data analysis by machine learning, and a great improvement in the training capabilities particularly of artificial deep neural networks (DNNs) inspired by the biological neural networks characterizing the human brain. This has generated competitive results for applications such as biomolecular target and protein structure prediction, structure-based rational drug design, and repurposing, all exerting a major impact on neuroscience and human well-being. By approaching early risks for diseases, non-invasive diagnosis, personalized treatment assessment, drug discovery, and automated science, the machine learning arena has thus the potential of becoming the new frontier for empowering neuroscience research and clinical practice in the years ahead. ,Cinzia Volonté [PublishedText] => Published [IsEdit] => 0 [AccountId] => 58 [Zh] => 1 [AuthorsName] => Cinzia Volonté ) [34] => Array ( [ArticleId] => 492 [Create_Time] => 2023-02-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202302/20230228022831.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100435/100435.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100435/100435.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100435/100435_cover.png [JournalsId] => 7 [Title] => Can chronic therapeutic drug use by the elderly affect Alzheimer’s disease risk and rate of progression? [Abstract] => There is no approved drug capable of halting the progression of the most prevalent neurodegenerative disorders, namely Alzheimer's disease (AD) and Parkinson's disease (PD). [AbstractComplete] =>

There is no approved drug capable of halting the progression of the most prevalent neurodegenerative disorders, namely Alzheimer’s disease (AD) and Parkinson’s disease (PD). Current therapeutic strategies focus mainly on the inhibition of the formation of protein aggregates and their deposition in the central nervous system. However, after almost a hundred years, proper management of the disease is still lacking. The fact of not finding effective management tools in the various clinical trials already carried out suggests that new hypotheses and strategies should be explored. Although vast resources have been allocated to the investigation of protein aggregates and the pathophysiology is now better understood, clues to the actual etiology are lacking. It is well known that brain homeostasis is of paramount importance for the survival of neurons. Drugs that target the periphery are often not subject to evaluation for their potential effect on the central nervous system. While acute treatments may be irrelevant, pills used for chronic conditions can be detrimental to neurons, especially in terms of progressive damage leading to a long-term decline in neuronal survival. Due to the lack of advances in the search for a curative treatment for neurodegenerative diseases, and the lack of new hypotheses about their etiology, a novel hypothesis is here proposed. It consists of assuming that the effects of the drugs most commonly used by the elderly, such as antihypertensive, hypoglycemic, and hypocholesterolemic, could have a negative impact on neuronal survival.

[Names] => Rafael Franco, Joan Serrano-Marín [CName] => [Doi] => 10.37349/ent.2023.00035 [Published] => February 27, 2023 [Viewed] => 1084 [Downloaded] => 31 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00035 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 135 [TitleAbbr] => Explor Neuroprot Ther [Pages] => 2023;3:8–23 [Recommend] => 0 [Keywords] => Diabetes, hypercholesterolemia, chronic diseases, overmedication, hypertension, cerebral blood flow, neurodegenerative diseases, musicians [DetailTitle] => The Urgent Need for New Hypotheses to Develop Effective Therapeutic Tools Against Alzheimers Disease [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/135 [Id] => 100435 [ris] => https://www.explorationpub.com/uploads/Article/A100435/7bae822e62b37175db9c256a67f36982.ris [bib] => https://www.explorationpub.com/uploads/Article/A100435/a5937e7fa005137114ed5a7cf4f0590f.bib [ens] => [Cited] => 3 [Cited_Time] => 2024-05-27 [CitethisArticle] => Franco R, Serrano-Marín J. Can chronic therapeutic drug use by the elderly affect Alzheimer’s disease risk and rate of progression? Explor Neuroprot Ther. 2023;3:8–23. https://doi.org/10.37349/ent.2023.00035 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-02-28 00:44:35 [Bib_Time] => 2023-02-25 00:58:29 [KeysWordContens] => Can chronic therapeutic drug use by the elderly affect Alzheimer’s disease risk and rate of progression?, Diabetes, hypercholesterolemia, chronic diseases, overmedication, hypertension, cerebral blood flow, neurodegenerative diseases, musicians, There is no approved drug capable of halting the progression of the most prevalent neurodegenerative disorders, namely Alzheimer’s disease (AD) and Parkinson’s disease (PD). Current therapeutic strategies focus mainly on the inhibition of the formation of protein aggregates and their deposition in the central nervous system. However, after almost a hundred years, proper management of the disease is still lacking. The fact of not finding effective management tools in the various clinical trials already carried out suggests that new hypotheses and strategies should be explored. Although vast resources have been allocated to the investigation of protein aggregates and the pathophysiology is now better understood, clues to the actual etiology are lacking. It is well known that brain homeostasis is of paramount importance for the survival of neurons. Drugs that target the periphery are often not subject to evaluation for their potential effect on the central nervous system. While acute treatments may be irrelevant, pills used for chronic conditions can be detrimental to neurons, especially in terms of progressive damage leading to a long-term decline in neuronal survival. Due to the lack of advances in the search for a curative treatment for neurodegenerative diseases, and the lack of new hypotheses about their etiology, a novel hypothesis is here proposed. It consists of assuming that the effects of the drugs most commonly used by the elderly, such as antihypertensive, hypoglycemic, and hypocholesterolemic, could have a negative impact on neuronal survival. ,Rafael Franco, Joan Serrano-Marín [PublishedText] => Published [IsEdit] => 0 [AccountId] => 46 [Zh] => 1 [AuthorsName] => Rafael Franco, Joan Serrano-Marín ) [35] => Array ( [ArticleId] => 498 [Create_Time] => 2023-02-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202302/20230228024733.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100436/100436.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100436/100436.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100436/100436_cover.png [JournalsId] => 7 [Title] => Pathophysiology of non-motor signs in Parkinson’s disease: some recent updating with brief presentation [Abstract] => Parkinson’s disease (PD) is a progressive neurodegenerative disorder affecting 1% of the population above sixty years. It is caused by an interaction between genetic and envi [AbstractComplete] =>

Parkinson’s disease (PD) is a progressive neurodegenerative disorder affecting 1% of the population above sixty years. It is caused by an interaction between genetic and environmental risk factors. Loss of dopaminergic neurons in substantia nigra pars compacta (SNpc) is pathologically characterizing the disease and responsible for the cardinal motor symptoms, most notably, bradykinesia, rest tremors, rigidity, and loss of postural reflexes. Non-motor signs such as olfactory deficits, cognitive impairment, sleep behavior disorders, and gastrointestinal disturbances are reflecting disturbances in the non-dopaminergic system. They precede dopaminergic neuronal degenerations by 5–10 years and are considered the main contributors to patients’ disability, particularly after the successful implementation of levodopa (L-dopa) treatment of motor symptoms. The present general review aimed to briefly update non-motor signs and their underlying pathophysiology in PD.

[Names] => Khaled Radad ... Wolf-Dieter Rausch [CName] => [Doi] => 10.37349/ent.2023.00036 [Published] => February 27, 2023 [Viewed] => 1182 [Downloaded] => 54 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00036 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 118 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:24–46 [Recommend] => 0 [Keywords] => Parkinson’s disease, non-motor signs, olfactory, depression, sleep disorders, constipation [DetailTitle] => Parkinsons Disease: Principal Targets and Interventional Mechanisms [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/118 [Id] => 100436 [ris] => https://www.explorationpub.com/uploads/Article/A100436/a405d0034a65b82eba79103681a0e067.ris [bib] => https://www.explorationpub.com/uploads/Article/A100436/9c588eedc27b32e816647bddfa4dd442.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Radad K, Moldzio R, Krewenka C, Kranner B, Rausch WD. Pathophysiology of non-motor signs in Parkinson’s disease: some recent updating with brief presentation. Explor Neuroprot Ther. 2023;3:24–46. https://doi.org/10.37349/ent.2023.00036 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-02-27 03:57:17 [Bib_Time] => 2023-02-27 03:57:17 [KeysWordContens] => Pathophysiology of non-motor signs in Parkinson’s disease: some recent updating with brief presentation, Parkinson’s disease, non-motor signs, olfactory, depression, sleep disorders, constipation, Parkinson’s disease (PD) is a progressive neurodegenerative disorder affecting 1% of the population above sixty years. It is caused by an interaction between genetic and environmental risk factors. Loss of dopaminergic neurons in substantia nigra pars compacta (SNpc) is pathologically characterizing the disease and responsible for the cardinal motor symptoms, most notably, bradykinesia, rest tremors, rigidity, and loss of postural reflexes. Non-motor signs such as olfactory deficits, cognitive impairment, sleep behavior disorders, and gastrointestinal disturbances are reflecting disturbances in the non-dopaminergic system. They precede dopaminergic neuronal degenerations by 5–10 years and are considered the main contributors to patients’ disability, particularly after the successful implementation of levodopa (L-dopa) treatment of motor symptoms. The present general review aimed to briefly update non-motor signs and their underlying pathophysiology in PD. ,Khaled Radad ... Wolf-Dieter Rausch [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 [AuthorsName] => Khaled Radad, Rudolf Moldzio, Christopher Krewenka, Barbara Kranner, Wolf-Dieter Rausch ) [36] => Array ( [ArticleId] => 511 [Create_Time] => 2023-03-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230613070449.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100437/100437.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100437/100437.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100437/100437_cover.png [JournalsId] => 7 [Title] => Neuroprotective agents in acute ischemic stroke [Abstract] => Acute ischemic stroke (AIS) is the leading cause of disability and one of the top causes of mortality worldwide. The current standard of care is reperfusion therapy including intravenous thrombolysi [AbstractComplete] =>

Acute ischemic stroke (AIS) is the leading cause of disability and one of the top causes of mortality worldwide. The current standard of care is reperfusion therapy including intravenous thrombolysis (IVT) and thrombectomy. However, these treatments have limitations as they have a limited therapeutic window. Hence, there is a vital need to develop neuroprotective agents to prevent brain injury, extend the reperfusion window, improve mortality, and reduce disability in AIS patients. Neuroprotective agents work by counteracting the detrimental biochemical and molecular events that result in irreversible ischemic damage. Numerous preclinical studies and clinical trials have been done on different agents. Thus far, all have been definitively unsuccessful in large trials. Currently, there are several challenges in translation from animal studies to human trials. It is important to understand the current evidence as well as past challenges in the development of neuroprotective strategies in AIS in order for a more strategic selection of agents to be studied, improve study designs and thus contribute to the development of effective neuroprotective agents. Newer agents have shown promise in neuroprotection, and human trials are ongoing. In this review, the mechanisms of action of different families of neuroprotective agents were discussed. The evidence for the efficacy of different drugs in each family of neuroprotective agents was also evaluated and the current research landscape in neuroprotection for AIS was summarized. The past challenges and limitations in clinical trials and proposed possible ways to address these issues were highlighted.

[Names] => Grace YY Chia ... Benjamin YQ Tan [CName] => Benjamin YQTan, [Doi] => 10.37349/ent.2023.00037 [Published] => February 28, 2023 [Viewed] => 2097 [Downloaded] => 88 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00037 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 79 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:47–70 [Recommend] => 0 [Keywords] => Neuroprotection, acute ischemic stroke, neuron death, therapeutic, mechanisms [DetailTitle] => The Future of Biomarkers in CNS Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/79 [Id] => 100437 [ris] => https://www.explorationpub.com/uploads/Article/A100437/141a64b65d6064f654d004751678d4bd.ris [bib] => https://www.explorationpub.com/uploads/Article/A100437/cc19c05524b578bea720b828e586407a.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-05-27 [CitethisArticle] => Chia GYY, Yeo S, Ho JSY, Jou E, Yeo LLL, Tan BYQ. Neuroprotective agents in acute ischemic stroke. Explor Neuroprot Ther. 2023;3:47–70. https://doi.org/10.37349/ent.2023.00037 [Jindex] => 0 [CEmail] => benjamin_yq_tan@nuhs.edu.sg, [Ris_Time] => 2023-02-27 03:43:40 [Bib_Time] => 2023-02-27 03:43:40 [KeysWordContens] => Neuroprotective agents in acute ischemic stroke, Neuroprotection, acute ischemic stroke, neuron death, therapeutic, mechanisms, Acute ischemic stroke (AIS) is the leading cause of disability and one of the top causes of mortality worldwide. The current standard of care is reperfusion therapy including intravenous thrombolysis (IVT) and thrombectomy. However, these treatments have limitations as they have a limited therapeutic window. Hence, there is a vital need to develop neuroprotective agents to prevent brain injury, extend the reperfusion window, improve mortality, and reduce disability in AIS patients. Neuroprotective agents work by counteracting the detrimental biochemical and molecular events that result in irreversible ischemic damage. Numerous preclinical studies and clinical trials have been done on different agents. Thus far, all have been definitively unsuccessful in large trials. Currently, there are several challenges in translation from animal studies to human trials. It is important to understand the current evidence as well as past challenges in the development of neuroprotective strategies in AIS in order for a more strategic selection of agents to be studied, improve study designs and thus contribute to the development of effective neuroprotective agents. Newer agents have shown promise in neuroprotection, and human trials are ongoing. In this review, the mechanisms of action of different families of neuroprotective agents were discussed. The evidence for the efficacy of different drugs in each family of neuroprotective agents was also evaluated and the current research landscape in neuroprotection for AIS was summarized. The past challenges and limitations in clinical trials and proposed possible ways to address these issues were highlighted. ,Grace YY Chia ... Benjamin YQ Tan [PublishedText] => Published [IsEdit] => 0 [AccountId] => 38 [Zh] => 1 [AuthorsName] => Grace YY Chia, Selvie Yeo, Jamie SY Ho, Eric Jou, Leonard LL Yeo, Benjamin YQ Tan ) [37] => Array ( [ArticleId] => 520 [Create_Time] => 2023-03-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202303/20230329085037.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100438/100438.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100438/100438.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100438/100438_cover.png [JournalsId] => 7 [Title] => The role of microbiota-gut-brain axis in neurodegenerative diseases: biochemical and therapeutic aspects [Abstract] => The enteric nervous system (ENS) is considered by some authors as the second human brain, given its fundamental role in the regulation process of the central nervous system (CNS). Recent data from s [AbstractComplete] =>

The enteric nervous system (ENS) is considered by some authors as the second human brain, given its fundamental role in the regulation process of the central nervous system (CNS). Recent data from scientific literature have shown the existence of close bidirectional communication between the gut microbiota and the CNS, influencing physiological and biochemical changes related to cognition, emotion, behavior, anxiety, depressive symptoms, and stress. Furthermore, the existence of mediators in the connection between intestinal microorganisms and the CNS is evident, which includes neural networks, signaling, immune, and endocrine responses. However, the mechanisms underlying the effects of gut microbiota on brain processes still need to be determined. Therefore, understanding the relationship between the gut and neurodegenerative diseases (NDs) is essential for developing effective prophylactic alternatives and disease-modifying drugs that can prevent or slow the progression of such diseases. Herein, this short review aimed to present the most recent data from the scientific literature associated with the physiological, biochemical, and cellular aspects involved in the interrelationship between the gut-brain axis and NDs, discussing the role of the intestinal microbiota, and its relationship with CNS disorders.

[Names] => Januário T. Ernesto ... Cláudio Viegas Jr. [CName] => [Doi] => 10.37349/ent.2023.00038 [Published] => March 29, 2023 [Viewed] => 1304 [Downloaded] => 51 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00038 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:71–89 [Recommend] => 0 [Keywords] => Microbiota-gut-brain axis, dysbiosis, neurodegenerative diseases [DetailTitle] => [DetailUrl] => [Id] => 100438 [ris] => https://www.explorationpub.com/uploads/Article/A100438/a151a0d9034df6426568d839527294c2.ris [bib] => https://www.explorationpub.com/uploads/Article/A100438/e1c20704a4de6b60152efa1054d4b281.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Ernesto JT, Damasio CM, Gontijo VS, Gasparotto J, Viegas C Jr. The role of microbiota-gut-brain axis in neurodegenerative diseases: biochemical and therapeutic aspects. Explor Neuroprot Ther. 2023;3:71–89. https://doi.org/10.37349/ent.2023.00038 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-03-29 01:20:34 [Bib_Time] => 2023-03-29 01:20:34 [KeysWordContens] => The role of microbiota-gut-brain axis in neurodegenerative diseases: biochemical and therapeutic aspects, Microbiota-gut-brain axis, dysbiosis, neurodegenerative diseases, The enteric nervous system (ENS) is considered by some authors as the second human brain, given its fundamental role in the regulation process of the central nervous system (CNS). Recent data from scientific literature have shown the existence of close bidirectional communication between the gut microbiota and the CNS, influencing physiological and biochemical changes related to cognition, emotion, behavior, anxiety, depressive symptoms, and stress. Furthermore, the existence of mediators in the connection between intestinal microorganisms and the CNS is evident, which includes neural networks, signaling, immune, and endocrine responses. However, the mechanisms underlying the effects of gut microbiota on brain processes still need to be determined. Therefore, understanding the relationship between the gut and neurodegenerative diseases (NDs) is essential for developing effective prophylactic alternatives and disease-modifying drugs that can prevent or slow the progression of such diseases. Herein, this short review aimed to present the most recent data from the scientific literature associated with the physiological, biochemical, and cellular aspects involved in the interrelationship between the gut-brain axis and NDs, discussing the role of the intestinal microbiota, and its relationship with CNS disorders. ,Januário T. Ernesto ... Cláudio Viegas Jr. [PublishedText] => Published [IsEdit] => 0 [AccountId] => 57 [Zh] => 1 [AuthorsName] => Januário T. Ernesto, Caio M. Damásio, Vanessa S. Gontijo, Juciano Gasparotto, Cláudio Viegas Jr. ) [38] => Array ( [ArticleId] => 521 [Create_Time] => 2023-04-03 [zipUrl] => https://www.explorationpub.com/uploads/zip/202304/20230404052309.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100439/100439.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100439/100439.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100439/100439_cover.png [JournalsId] => 7 [Title] => Innate and adaptive glial cell responses in Alzheimer’s disease [Abstract] => Alzheimer’s disease (AD), which affects around twenty-seven million people globally, is an aging-related neurodegenerative condition characterized by the extracellular deposition of misfolded amyl [AbstractComplete] =>

Alzheimer’s disease (AD), which affects around twenty-seven million people globally, is an aging-related neurodegenerative condition characterized by the extracellular deposition of misfolded amyloid-β (Aβ) peptides and the intracellular production of neurofibrillary tangles (NFTs) AD results from the death of certain groups of neurons in the brain while appearing to have no impact on neighboring neurons. It is progressive and incurable. Therefore, the pathophysiology of afflicted populations and the development of intervention measures to stop neuronal cell death have been the main areas of attention for delineating therapeutic options. Proinflammatory cytokines are responsible for the stimulation of inflammatory responses and are mostly generated by activated macrophages in the brain. This review discusses how glial cells and innate and adaptive immune responses have a critical role in AD. It also provides information about microglial activation through the cluster of differentiation 40 (CD40) ligation and CD40L. CD40L ligation of microglial CD40 results in a large increase in tumor necrosis factor-α (TNF-α) production. Cultured cortical neuronal injury is caused when microglia are activated by CD40 ligation in the presence of interferon-γ (IFN-γ). This injury is significantly reduced by blocking the CD40 pathway or neutralising TNF-α. The management of AD would require integrating all available information about the innate and adaptive immune response affecting AD-related neuronal death.

[Names] => Ankita Singh, Tiratha Raj Singh [CName] => [Doi] => 10.37349/ent.2023.00039 [Published] => April 03, 2023 [Viewed] => 1137 [Downloaded] => 33 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00039 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 74 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:90–104 [Recommend] => 0 [Keywords] => Alzheimer’s disease, neurodegenerative disease, aging, innate, adaptive, glia [DetailTitle] => Glia and Neuroprotection [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/74 [Id] => 100439 [ris] => https://www.explorationpub.com/uploads/Article/A100439/9f47b00ee7b6b31488c308b1026e4eee.ris [bib] => https://www.explorationpub.com/uploads/Article/A100439/b59268692ff20ccd77e950eedd3445bc.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Singh A, Singh TR. Innate and adaptive glial cell responses in Alzheimer’s disease. Explor Neuroprot Ther. 2023;3:90–104. https://doi.org/10.37349/ent.2023.00039 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-03-23 06:24:21 [Bib_Time] => 2023-03-23 06:24:21 [KeysWordContens] => Innate and adaptive glial cell responses in Alzheimer’s disease, Alzheimer’s disease, neurodegenerative disease, aging, innate, adaptive, glia, Alzheimer’s disease (AD), which affects around twenty-seven million people globally, is an aging-related neurodegenerative condition characterized by the extracellular deposition of misfolded amyloid-β (Aβ) peptides and the intracellular production of neurofibrillary tangles (NFTs) AD results from the death of certain groups of neurons in the brain while appearing to have no impact on neighboring neurons. It is progressive and incurable. Therefore, the pathophysiology of afflicted populations and the development of intervention measures to stop neuronal cell death have been the main areas of attention for delineating therapeutic options. Proinflammatory cytokines are responsible for the stimulation of inflammatory responses and are mostly generated by activated macrophages in the brain. This review discusses how glial cells and innate and adaptive immune responses have a critical role in AD. It also provides information about microglial activation through the cluster of differentiation 40 (CD40) ligation and CD40L. CD40L ligation of microglial CD40 results in a large increase in tumor necrosis factor-α (TNF-α) production. Cultured cortical neuronal injury is caused when microglia are activated by CD40 ligation in the presence of interferon-γ (IFN-γ). This injury is significantly reduced by blocking the CD40 pathway or neutralising TNF-α. The management of AD would require integrating all available information about the innate and adaptive immune response affecting AD-related neuronal death. ,Ankita Singh, Tiratha Raj Singh [PublishedText] => Published [IsEdit] => 0 [AccountId] => 45 [Zh] => 1 [AuthorsName] => Ankita Singh, Tiratha Raj Singh ) [39] => Array ( [ArticleId] => 584 [Create_Time] => 2023-04-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202304/20230428051150.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100442/100442.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100442/100442.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100442/100442_cover.png [JournalsId] => 7 [Title] => Efficacy of memantine compared with sodium valproate as prophylactic treatment for migraine: a controlled randomized pilot study [Abstract] => Aim: To compare the efficacy of memantine with that of valproate as a prophylactic treatment for episodic migraine within three months. The efficacy, safety, and response rate were evaluated. [AbstractComplete] =>

Aim:

To compare the efficacy of memantine with that of valproate as a prophylactic treatment for episodic migraine within three months. The efficacy, safety, and response rate were evaluated.

Methods:

Prospective, randomized, double-blind, controlled clinical trial randomized participants were divided into two groups. The memantine group received memantine 10 mg twice daily, and the valproate group received valproate 500 mg twice daily.

Results:

Thirty-three patients participated in the study; 27 completed the treatment protocol, 14 in the memantine group, and 13 in the valproate group. The mean number of migraine attacks per month in the memantine group was 5.31 [standard deviation (SD) ± 1.54] initially and 0.93 (SD ± 1.49) at the end of treatment, noting a decrease of 4.21 (SD ± 1.76; P < 0.001). In the valproate group, the mean number of migraine attacks per month was 5.35 (SD ± 1.11) initially and 0.77 (SD ± 1.16) at the end of treatment, with a difference of 4.5 (SD ± 1.39; P < 0.001). All 27 patients had excellent response rates. Adverse effects were infrequent and mild in severity.

Conclusions:

A clinical trial compared the efficacy of memantine with that of valproate (first-line drug) as a prophylactic treatment. A significant reduction in attacks was noted in both drugs. Memantine could be a new preventive treatment option for migraine (ClinicalTrials.gov identifier: NCT04698525).

[Names] => Damaris Vazquez-Guevara ... Ildefonso Rodriguez-Leyva [CName] => [Doi] => 10.37349/ent.2023.00042 [Published] => April 28, 2023 [Viewed] => 781 [Downloaded] => 21 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00042 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:131–138 [Recommend] => 0 [Keywords] => Memantine, valproate, prophylactic treatment, episodic migraine, efficacy, safety [DetailTitle] => [DetailUrl] => [Id] => 100442 [ris] => https://www.explorationpub.com/uploads/Article/A100442/a1a6c524304e7eefa4c0914b20577c84.ris [bib] => https://www.explorationpub.com/uploads/Article/A100442/a0bfe46356525aaeddb4f28eb7bc9e78.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Vazquez-Guevara D, Orozco-Narvaez A, Hernandez-Rodriguez HG, Rivas-Ruvalcaba F, Shiguetomi-Medina JM, Rodriguez-Leyva I. Efficacy of memantine compared with sodium valproate as prophylactic treatment for migraine: a controlled randomized pilot study. Explor Neuroprot Ther. 2023;3:131–8. https://doi.org/10.37349/ent.2023.00042 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-04-28 05:01:38 [Bib_Time] => 2023-04-28 05:01:38 [KeysWordContens] => Efficacy of memantine compared with sodium valproate as prophylactic treatment for migraine: a controlled randomized pilot study, Memantine, valproate, prophylactic treatment, episodic migraine, efficacy, safety, Aim: To compare the efficacy of memantine with that of valproate as a prophylactic treatment for episodic migraine within three months. The efficacy, safety, and response rate were evaluated. Methods: Prospective, randomized, double-blind, controlled clinical trial randomized participants were divided into two groups. The memantine group received memantine 10 mg twice daily, and the valproate group received valproate 500 mg twice daily. Results: Thirty-three patients participated in the study; 27 completed the treatment protocol, 14 in the memantine group, and 13 in the valproate group. The mean number of migraine attacks per month in the memantine group was 5.31 [standard deviation (SD) ± 1.54] initially and 0.93 (SD ± 1.49) at the end of treatment, noting a decrease of 4.21 (SD ± 1.76; P < 0.001). In the valproate group, the mean number of migraine attacks per month was 5.35 (SD ± 1.11) initially and 0.77 (SD ± 1.16) at the end of treatment, with a difference of 4.5 (SD ± 1.39; P < 0.001). All 27 patients had excellent response rates. Adverse effects were infrequent and mild in severity. Conclusions: A clinical trial compared the efficacy of memantine with that of valproate (first-line drug) as a prophylactic treatment. A significant reduction in attacks was noted in both drugs. Memantine could be a new preventive treatment option for migraine (ClinicalTrials.gov identifier: NCT04698525). ,Damaris Vazquez-Guevara ... Ildefonso Rodriguez-Leyva [PublishedText] => Published [IsEdit] => 0 [AccountId] => 46 [Zh] => 1 [AuthorsName] => Damaris Vazquez-Guevara, Alejandro Orozco-Narvaez, Hector G. Hernandez-Rodriguez, Francisco Rivas-Ruvalcaba, Juan Manuel Shiguetomi-Medina, Ildefonso Rodriguez-Leyva ) [40] => Array ( [ArticleId] => 582 [Create_Time] => 2023-04-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230613050804.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100440/100440.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100440/100440.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100440/100440_cover.png [JournalsId] => 7 [Title] => Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease [Abstract] => Late-onset Alzheimer's disease (LOAD) is the most common form of Alzheimer's disease (AD) and its risk increases exponentially with aging. The incidence of LOAD is reported to [AbstractComplete] =>

Late-onset Alzheimer’s disease (LOAD) is the most common form of Alzheimer’s disease (AD) and its risk increases exponentially with aging. The incidence of LOAD is reported to increase from 1 in every 1,000 people aged 37 to 65 in every 100 people aged 80 years and older. LOAD is extensively associated with aging and cognition decline. Several risk factors, including lifestyle choices, environmental factors, and medical ailments, affect cellular stress. The cellular stress can bring upon epigenetic alterations that affect cellular aging making the individual more susceptible to LOAD development. In due course the cellular stress resulting into epigenetic deregulation, oxidative burden, and genomic mutations leads to increased disease risk. Role of epigenetic and non-epigenetic mechanisms in accelerated cellular aging that are reported to increase the risk of LOAD development are summarized in this review. The underlying biological mechanism of cellular aging and the risk factors that could predispose cellular aging and LOAD development are also discussed in the upcoming sections.

[Names] => Kajal Rawat, Prathiba Garlapally [CName] => KajalRawat, [Doi] => 10.37349/ent.2023.00040 [Published] => April 28, 2023 [Viewed] => 1020 [Downloaded] => 40 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00040 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 106 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:105–119 [Recommend] => 0 [Keywords] => Late-onset Alzheimer’s disease, epigenetics, cellular aging, telomere length, immunosensecence [DetailTitle] => Recent Advances in Neurochemistry and Genetics of Late-onset Alzheimer's Disease [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/106 [Id] => 100440 [ris] => https://www.explorationpub.com/uploads/Article/A100440/8678cfe26abf0c62f632219b023ec4c8.ris [bib] => https://www.explorationpub.com/uploads/Article/A100440/285d67d23ab6ce4dbf2da70a2607b1a9.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Rawat K, Garlapally P. Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease. Explor Neuroprot Ther. 2023;3:105–19. https://doi.org/10.37349/ent.2023.00040 [Jindex] => 0 [CEmail] => kaajjalrawat111@gmail.com, [Ris_Time] => 2023-04-27 11:01:26 [Bib_Time] => 2023-04-27 11:01:26 [KeysWordContens] => Epigenetic and non-epigenetic mechanisms in the accelerated cellular aging in late-onset Alzheimer’s disease, Late-onset Alzheimer’s disease, epigenetics, cellular aging, telomere length, immunosensecence, Late-onset Alzheimer’s disease (LOAD) is the most common form of Alzheimer’s disease (AD) and its risk increases exponentially with aging. The incidence of LOAD is reported to increase from 1 in every 1,000 people aged 37 to 65 in every 100 people aged 80 years and older. LOAD is extensively associated with aging and cognition decline. Several risk factors, including lifestyle choices, environmental factors, and medical ailments, affect cellular stress. The cellular stress can bring upon epigenetic alterations that affect cellular aging making the individual more susceptible to LOAD development. In due course the cellular stress resulting into epigenetic deregulation, oxidative burden, and genomic mutations leads to increased disease risk. Role of epigenetic and non-epigenetic mechanisms in accelerated cellular aging that are reported to increase the risk of LOAD development are summarized in this review. The underlying biological mechanism of cellular aging and the risk factors that could predispose cellular aging and LOAD development are also discussed in the upcoming sections. ,Kajal Rawat, Prathiba Garlapally [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 [AuthorsName] => Kajal Rawat, Prathiba Garlapally ) [41] => Array ( [ArticleId] => 583 [Create_Time] => 2023-04-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230809083655.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100441/100441.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100441/100441.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100441/100441_cover.png [JournalsId] => 7 [Title] => Reversible cerebral vasoconstriction syndrome: a clinical and therapeutic challenge [Abstract] => Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by thunderclap headache and intracranial segmental vasoconstriction with or without signs of neurological deficit with a variabl [AbstractComplete] =>

Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by thunderclap headache and intracranial segmental vasoconstriction with or without signs of neurological deficit with a variable course that requires extensive study to prevent complications. The evidence shows RCVS is characterized by being multi-etiological; both the cause and the specific symptoms must be treated to reduce the chance of complications and recurrence. The timely identification of the RCVS and its etiology is the cornerstone of success in managing the disease. New data must be generated to have more efficient resources for the approach to this disease.

[Names] => Andrés Ricaurte-Fajardo ... Nathalia Melo Gonzalez [CName] => AndrésRicaurte-Fajardo, [Doi] => 10.37349/ent.2023.00041 [Published] => April 28, 2023 [Viewed] => 963 [Downloaded] => 43 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00041 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 66 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:120–130 [Recommend] => 0 [Keywords] => Cerebral angiography, headache, subarachnoid hemorrhage, calcium channel blockers, magnetic resonance, reversible cerebral vasoconstriction syndrome [DetailTitle] => Emerging Concepts in Subarachnoid Hemorrhage [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/66 [Id] => 100441 [ris] => https://www.explorationpub.com/uploads/Article/A100441/a1a2f94b8c5ac4b471d16aac6620029e.ris [bib] => https://www.explorationpub.com/uploads/Article/A100441/998732d1a4ed79377975fde4edb77575.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Ricaurte-Fajardo A, Rodríguez Suarez L, Melo Gonzalez N. Reversible cerebral vasoconstriction syndrome: a clinical and therapeutic challenge. Explor Neuroprot Ther. 2023;3:120–30. https://doi.org/10.37349/ent.2023.00041 [Jindex] => 0 [CEmail] => andres.ricaurte@javeriana.edu.co, [Ris_Time] => 2023-04-27 08:26:43 [Bib_Time] => 2023-04-27 08:26:43 [KeysWordContens] => Reversible cerebral vasoconstriction syndrome: a clinical and therapeutic challenge, Cerebral angiography, headache, subarachnoid hemorrhage, calcium channel blockers, magnetic resonance, reversible cerebral vasoconstriction syndrome, Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by thunderclap headache and intracranial segmental vasoconstriction with or without signs of neurological deficit with a variable course that requires extensive study to prevent complications. The evidence shows RCVS is characterized by being multi-etiological; both the cause and the specific symptoms must be treated to reduce the chance of complications and recurrence. The timely identification of the RCVS and its etiology is the cornerstone of success in managing the disease. New data must be generated to have more efficient resources for the approach to this disease. ,Andrés Ricaurte-Fajardo ... Nathalia Melo Gonzalez [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 [AuthorsName] => Andrés Ricaurte-Fajardo, Laura Rodríguez Suarez, Nathalia Melo Gonzalez ) [42] => Array ( [ArticleId] => 626 [Create_Time] => 2023-06-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230630073649.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100443/100443.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100443/100443.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100443/100443_cover.png [JournalsId] => 7 [Title] => Alzheimer’s disease detection from magnetic resonance imaging: a deep learning perspective [Abstract] => Aim: Up to date many successful attempts to identify various types of lesions with machine learning (ML) were made, however, the recognition of Alzheimer’s disease (AD) from brain images and inter [AbstractComplete] =>

Aim:

Up to date many successful attempts to identify various types of lesions with machine learning (ML) were made, however, the recognition of Alzheimer’s disease (AD) from brain images and interpretation of the models is still a topic for the research. Here, using AD Imaging Initiative (ADNI) structural magnetic resonance imaging (MRI) brain images, the scope of this work was to find an optimal artificial neural network architecture for multiclass classification in AD, circumventing the dozens of images pre-processing steps and avoiding to increase the computational complexity.

Methods:

For this analysis, two supervised deep neural network (DNN) models were used, a three-dimensional 16-layer visual geometry-group (3D-VGG-16) standard convolutional network (CNN) and a three-dimensional residual network (ResNet3D) on the T1-weighted, 1.5 T ADNI MRI brain images that were divided into three groups: cognitively normal (CN), mild cognitive impairment (MCI), and AD. The minimal pre-processing procedure of the images was applied before training the two networks.

Results:

Results achieved suggest, that the network ResNet3D has a better performance in class prediction, which is higher than 90% in training set accuracy and arrives to 85% in validation set accuracy. ResNet3D also showed requiring less computational power than the 3D-VGG-16 network. The emphasis is also given to the fact that this result was achieved from raw images, applying minimal image preparation for the network.

Conclusions:

In this work, it has been shown that ResNet3D might have superiority over the other CNN models in the ability to classify high-complexity images. The prospective stands in doing a step further in creating an expert system based on residual DNNs for better brain image classification performance in AD detection.

[Names] => Karolina Armonaite ... Luigi Laura [CName] => [Doi] => 10.37349/ent.2023.00043 [Published] => June 30, 2023 [Viewed] => 1059 [Downloaded] => 48 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00043 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 135 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:139–150 [Recommend] => 0 [Keywords] => Convolutional neural networks, three-dimensional residual networks, expert system, Alzheimer’s disease [DetailTitle] => The Urgent Need for New Hypotheses to Develop Effective Therapeutic Tools Against Alzheimer's Disease [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/135 [Id] => 100443 [ris] => https://www.explorationpub.com/uploads/Article/A100443/3999f0b1c4ed791b4ec28683838f5874.ris [bib] => https://www.explorationpub.com/uploads/Article/A100443/1a7bcf972854e542a68c41850b71a215.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-05-27 [CitethisArticle] => Armonaite K, Ventura ML, Laura L. Alzheimer’s disease detection from magnetic resonance imaging: a deep learning perspective. Explor Neuroprot Ther. 2023;3:139–150. https://doi.org/10.37349/ent.2023.00043 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-06-29 08:30:32 [Bib_Time] => 2023-06-29 08:30:32 [KeysWordContens] => Alzheimer’s disease detection from magnetic resonance imaging: a deep learning perspective, Convolutional neural networks, three-dimensional residual networks, expert system, Alzheimer’s disease, Aim: Up to date many successful attempts to identify various types of lesions with machine learning (ML) were made, however, the recognition of Alzheimer’s disease (AD) from brain images and interpretation of the models is still a topic for the research. Here, using AD Imaging Initiative (ADNI) structural magnetic resonance imaging (MRI) brain images, the scope of this work was to find an optimal artificial neural network architecture for multiclass classification in AD, circumventing the dozens of images pre-processing steps and avoiding to increase the computational complexity. Methods: For this analysis, two supervised deep neural network (DNN) models were used, a three-dimensional 16-layer visual geometry-group (3D-VGG-16) standard convolutional network (CNN) and a three-dimensional residual network (ResNet3D) on the T1-weighted, 1.5 T ADNI MRI brain images that were divided into three groups: cognitively normal (CN), mild cognitive impairment (MCI), and AD. The minimal pre-processing procedure of the images was applied before training the two networks. Results: Results achieved suggest, that the network ResNet3D has a better performance in class prediction, which is higher than 90% in training set accuracy and arrives to 85% in validation set accuracy. ResNet3D also showed requiring less computational power than the 3D-VGG-16 network. The emphasis is also given to the fact that this result was achieved from raw images, applying minimal image preparation for the network. Conclusions: In this work, it has been shown that ResNet3D might have superiority over the other CNN models in the ability to classify high-complexity images. The prospective stands in doing a step further in creating an expert system based on residual DNNs for better brain image classification performance in AD detection. ,Karolina Armonaite ... Luigi Laura [PublishedText] => Published [IsEdit] => 0 [AccountId] => 46 [Zh] => 1 [AuthorsName] => Karolina Armonaite, Marco La Ventura, Luigi Laura ) [43] => Array ( [ArticleId] => 632 [Create_Time] => 2023-06-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230630101114.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100444/100444.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100444/100444.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100444/100444_cover.png [JournalsId] => 7 [Title] => Looking at the periphery—new hypothesis to look for new targets for Alzheimer’s disease therapy [Abstract] => Currently, the predominant targets for the treatment of Alzheimer’s disease (AD) are the main components of the two pathological structures: senile plaques (composed of amyloid beta peptide aggreg [AbstractComplete] =>

Currently, the predominant targets for the treatment of Alzheimer’s disease (AD) are the main components of the two pathological structures: senile plaques (composed of amyloid beta peptide aggregates) or neurofibrillary tangles (constructed of tau protein polymers). However, the existence of adequate disease modifiers based on such targets is discussed. In this special issue, it has been suggested to search for new possible targets for AD therapy. This contribution tries to analyze non-neuronal tissues (periphery) to identify potential factors (target) involved in the development of AD.

[Names] => Jesús Avila ... Félix Hernández [CName] => [Doi] => 10.37349/ent.2023.00044 [Published] => June 30, 2023 [Viewed] => 973 [Downloaded] => 42 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00044 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 135 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:151–163 [Recommend] => 0 [Keywords] => Alzheimer’s disease, non-neuronal tissues, biomarkers [DetailTitle] => The Urgent Need for New Hypotheses to Develop Effective Therapeutic Tools Against Alzheimer's Disease [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/135 [Id] => 100444 [ris] => https://www.explorationpub.com/uploads/Article/A100444/cb1efe64dfd186da4b1f05c794ca1eb9.ris [bib] => https://www.explorationpub.com/uploads/Article/A100444/6a86a03489c2fa96b6cfdb55c4f691fd.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Avila J, Pérez M, Avila-Villanueva M, Santa-María I, Hernández F. Looking at the periphery—new hypothesis to look for new targets for Alzheimer’s disease therapy. Explor Neuroprot Ther. 2023;3:151–63. https://doi.org/10.37349/ent.2023.00044 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-06-30 03:27:45 [Bib_Time] => 2023-06-30 00:49:06 [KeysWordContens] => Looking at the periphery—new hypothesis to look for new targets for Alzheimer’s disease therapy, Alzheimer’s disease, non-neuronal tissues, biomarkers, Currently, the predominant targets for the treatment of Alzheimer’s disease (AD) are the main components of the two pathological structures: senile plaques (composed of amyloid beta peptide aggregates) or neurofibrillary tangles (constructed of tau protein polymers). However, the existence of adequate disease modifiers based on such targets is discussed. In this special issue, it has been suggested to search for new possible targets for AD therapy. This contribution tries to analyze non-neuronal tissues (periphery) to identify potential factors (target) involved in the development of AD. ,Jesús Avila ... Félix Hernández [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 1 [AuthorsName] => Jesús Avila, Mar Pérez, Marina Avila-Villanueva, Ismael Santa-María, Félix Hernández ) [44] => Array ( [ArticleId] => 633 [Create_Time] => 2023-06-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230630103821.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100445/100445.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100445/100445.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100445/100445_cover.png [JournalsId] => 7 [Title] => Muscle fatigue and exercise-related biomarkers in amyotrophic lateral sclerosis [Abstract] => Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder affecting motor neurons. The complex etiopathogenetic mechanism of ALS can lead to extensive alterations, including co [AbstractComplete] =>

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder affecting motor neurons. The complex etiopathogenetic mechanism of ALS can lead to extensive alterations, including cortical changes, neuroinflammation, and changes in muscular structure. These ALS-derived alterations may contribute to fatigue, a symptom severely impacting patients’ quality of life that is commonly associated with muscular exercise. Intriguingly, muscular exercise can be at once a promoter of motor neuron degeneration in predisposed patients as well as an effective non-pharmacological treatment of ALS. To fully disclose its therapeutic potential, muscular exercise must be tailored to patients’ phenotypes, balancing potential benefits and risks that are unique to each ALS case. Biomarkers of muscular fatigue, with their potential for insight into inflammation and oxidation, can be used to ensure that the intensity of physical activity remains below the threshold level beyond which exercise might become harmful. In this review, the authors explore the concept of fatigue in ALS patients, focusing on fatigue generation, definition, detection, quantification, and treatment. The study discusses the most important fatigue biomarkers, putting them in relation to the mechanism of fatigue generation and with monitoring of muscular exercise as a possible treatment of fatigue.

[Names] => Francesca Bianchi ... Gabriele Siciliano [CName] => [Doi] => 10.37349/ent.2023.00045 [Published] => June 30, 2023 [Viewed] => 761 [Downloaded] => 28 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00045 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 89 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:164–176 [Recommend] => 0 [Keywords] => Amyotrophic lateral sclerosis (ALS), fatigue, biomarkers, muscular exercise [DetailTitle] => Biomarkers in Amyotrophic Lateral Sclerosis [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/89 [Id] => 100445 [ris] => https://www.explorationpub.com/uploads/Article/A100445/470cdd8d43d8d7e7b6b73b2b8c9f99b5.ris [bib] => https://www.explorationpub.com/uploads/Article/A100445/b465cd7d2c97ef3f9852b601fc26a2a5.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Bianchi F, Becattini L, Chico L, Ricci G, Siciliano G. Muscle fatigue and exercise-related biomarkers in amyotrophic lateral sclerosis. Explor Neuroprot Ther. 2023;3:164–76. https://doi.org/10.37349/ent.2023.00045 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-06-30 01:09:34 [Bib_Time] => 2023-06-30 01:09:34 [KeysWordContens] => Muscle fatigue and exercise-related biomarkers in amyotrophic lateral sclerosis, Amyotrophic lateral sclerosis (ALS), fatigue, biomarkers, muscular exercise, Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder affecting motor neurons. The complex etiopathogenetic mechanism of ALS can lead to extensive alterations, including cortical changes, neuroinflammation, and changes in muscular structure. These ALS-derived alterations may contribute to fatigue, a symptom severely impacting patients’ quality of life that is commonly associated with muscular exercise. Intriguingly, muscular exercise can be at once a promoter of motor neuron degeneration in predisposed patients as well as an effective non-pharmacological treatment of ALS. To fully disclose its therapeutic potential, muscular exercise must be tailored to patients’ phenotypes, balancing potential benefits and risks that are unique to each ALS case. Biomarkers of muscular fatigue, with their potential for insight into inflammation and oxidation, can be used to ensure that the intensity of physical activity remains below the threshold level beyond which exercise might become harmful. In this review, the authors explore the concept of fatigue in ALS patients, focusing on fatigue generation, definition, detection, quantification, and treatment. The study discusses the most important fatigue biomarkers, putting them in relation to the mechanism of fatigue generation and with monitoring of muscular exercise as a possible treatment of fatigue. ,Francesca Bianchi ... Gabriele Siciliano [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 [AuthorsName] => Francesca Bianchi, Lucrezia Becattini, Lucia Chico, Giulia Ricci, Gabriele Siciliano ) [45] => Array ( [ArticleId] => 698 [Create_Time] => 2023-08-25 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230828015011.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100448/100448.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100448/100448.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100448/100448_cover.png [JournalsId] => 7 [Title] => Targeting α-synuclein aggregation with immunotherapy: a promising therapeutic approach for Parkinson’s disease [Abstract] => Parkinson’s disease (PD) is a prevalent neurodegenerative disease (NDD) affecting millions of individuals. The pathogenesis of PD centers around α-synuclein (α-Syn), a pivotal protein whose aggr [AbstractComplete] =>

Parkinson’s disease (PD) is a prevalent neurodegenerative disease (NDD) affecting millions of individuals. The pathogenesis of PD centers around α-synuclein (α-Syn), a pivotal protein whose aggregation significantly impacts disease progression. Although existing treatments mainly focus on managing motor symptoms by targeting the dopaminergic system, they frequently overlook other non-motor symptoms. The intricate nature of PD pathogenesis contributes to challenges in disease analysis and has hindered the development of effective PD treatments. In recent years, various novel therapies utilizing immunotherapy methods have exhibited promise in preclinical animal models. In NDDs, immunotherapy aims to counteract the detrimental effects of protein accumulation by neutralizing toxic species and aiding their elimination. Numerous active therapy (AI) and passive immunotherapy (PI) strategies have been devised for PD and related synucleinopathies, many of which are currently undergoing clinical trials. Despite demonstrating remarkable success in animal models, immunotherapies encountered substantial setbacks during the late stages of clinical trials, with the exception of lecanemab, which targets amyloid-β (Aβ) in Alzheimer’s disease (AD) and has recently received approval from the Food and Drug Administration (FDA). The lack of translation from experimental investigations to successful clinical outcomes, particularly in terms of cognitive and functional evaluations, highlights the limitations of relying solely on animal studies to comprehend the effects of immunotherapeutic approaches. This comprehensive review focuses on α-Syn-based immunotherapies and delves into their underlying mechanisms of action. Furthermore, Furthermore, the article discusses recent advancements and future prospects concerning the potential of immunotherapeutic strategies for PD. The focus is on highlighting the latest research in this domain to illuminate the challenges and opportunities related to the development of efficacious immunotherapies for individuals with PD.

[Names] => Gabriela Henriquez, Mahesh Narayan [CName] => [Doi] => 10.37349/ent.2023.00048 [Published] => August 25, 2023 [Viewed] => 1329 [Downloaded] => 56 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00048 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 118 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:207–234 [Recommend] => 0 [Keywords] => Parkinson’s disease, α-synuclein, immunotherapy, misfolded protein, preclinical, clinical trial, synucleinopathies, neurodegenerative disease [DetailTitle] => Parkinsons Disease: Principal Targets and Interventional Mechanisms [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/118 [Id] => 100448 [ris] => https://www.explorationpub.com/uploads/Article/A100448/b9c0ccd46307027552c0495691a46ed8.ris [bib] => https://www.explorationpub.com/uploads/Article/A100448/47916d261a0a52c8223ae0916073d5fe.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Henriquez G, Narayan M. Targeting α-synuclein aggregation with immunotherapy: a promising therapeutic approach for Parkinson’s disease. Explor Neuroprot Ther. 2023;3:207–34. https://doi.org/10.37349/ent.2023.00048 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-08-22 06:25:51 [Bib_Time] => 2023-08-22 06:25:51 [KeysWordContens] => Targeting α-synuclein aggregation with immunotherapy: a promising therapeutic approach for Parkinson’s disease, Parkinson’s disease, α-synuclein, immunotherapy, misfolded protein, preclinical, clinical trial, synucleinopathies, neurodegenerative disease, Parkinson’s disease (PD) is a prevalent neurodegenerative disease (NDD) affecting millions of individuals. The pathogenesis of PD centers around α-synuclein (α-Syn), a pivotal protein whose aggregation significantly impacts disease progression. Although existing treatments mainly focus on managing motor symptoms by targeting the dopaminergic system, they frequently overlook other non-motor symptoms. The intricate nature of PD pathogenesis contributes to challenges in disease analysis and has hindered the development of effective PD treatments. In recent years, various novel therapies utilizing immunotherapy methods have exhibited promise in preclinical animal models. In NDDs, immunotherapy aims to counteract the detrimental effects of protein accumulation by neutralizing toxic species and aiding their elimination. Numerous active therapy (AI) and passive immunotherapy (PI) strategies have been devised for PD and related synucleinopathies, many of which are currently undergoing clinical trials. Despite demonstrating remarkable success in animal models, immunotherapies encountered substantial setbacks during the late stages of clinical trials, with the exception of lecanemab, which targets amyloid-β (Aβ) in Alzheimer’s disease (AD) and has recently received approval from the Food and Drug Administration (FDA). The lack of translation from experimental investigations to successful clinical outcomes, particularly in terms of cognitive and functional evaluations, highlights the limitations of relying solely on animal studies to comprehend the effects of immunotherapeutic approaches. This comprehensive review focuses on α-Syn-based immunotherapies and delves into their underlying mechanisms of action. Furthermore, Furthermore, the article discusses recent advancements and future prospects concerning the potential of immunotherapeutic strategies for PD. The focus is on highlighting the latest research in this domain to illuminate the challenges and opportunities related to the development of efficacious immunotherapies for individuals with PD. ,Gabriela Henriquez, Mahesh Narayan [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 [AuthorsName] => Gabriela Henriquez, Mahesh Narayan ) [46] => Array ( [ArticleId] => 697 [Create_Time] => 2023-08-25 [zipUrl] => https://www.explorationpub.com/uploads/zip/202401/20240104065751.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100447/100447.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100447/100447.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100447/100447_cover.png [JournalsId] => 7 [Title] => Retracted: Diffusion magnetic resonance imaging-based surrogate marker in amyotrophic lateral sclerosis [Abstract] => Amyotrophic lateral sclerosis (ALS) is the most prevalent type of motor neuron disease (MND) and is diagnosed with a delay from the first appearance of symptoms. Surrogate markers that may be used t [AbstractComplete] =>

Amyotrophic lateral sclerosis (ALS) is the most prevalent type of motor neuron disease (MND) and is diagnosed with a delay from the first appearance of symptoms. Surrogate markers that may be used to detect pathological changes before a significant neuronal loss occurs and allow for early intervention with disease-modifying therapy techniques are desperately needed. Using water molecules that diffuse within the tissue and experience displacement on the micron scale, diffusion magnetic resonance imaging (MRI) is a promising technique that can be used to infer microstructural characteristics of the brain, such as microstructural integrity and complexity, axonal density, order, and myelination. Diffusion tensor imaging (DTI) is the primary diffusion MRI technique used to evaluate the pathogenesis of ALS. Neurite orientation dispersion and density imaging (NODDI), diffusion kurtosis imaging (DKI), and free water elimination DTI (FWE-DTI) are only a few of the approaches that have been developed to overcome the shortcomings of the diffusion tensor technique. This article provides a summary of these methods and their potential as surrogate markers for detecting the onset of ALS at an early stage.

[Names] => Yuya Saito [CName] => YuyaSaito, [Doi] => 10.37349/ent.2023.00047 [Published] => August 25, 2023 [Viewed] => 809 [Downloaded] => 30 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00047 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 89 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:186–206 [Recommend] => 0 [Keywords] => Amyotrophic lateral sclerosis, surrogate marker, diffusion kurtosis imaging, diffusion tensor imaging, free water elimination diffusion tensor imaging, neurite orientation dispersion and density imaging [DetailTitle] => Biomarkers in Amyotrophic Lateral Sclerosis [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/89 [Id] => 100447 [ris] => https://www.explorationpub.com/uploads/Article/A100447/5ac5a992d02a2a5908c6dbf637b92eeb.ris [bib] => https://www.explorationpub.com/uploads/Article/A100447/75b4daef6f0a19e89d9a58eed0010cdb.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-05-27 [CitethisArticle] => Saito Y. Diffusion magnetic resonance imaging-based surrogate marker in amyotrophic lateral sclerosis. Explor Neuroprot Ther. 2023;3:186–206. https://doi.org/10.37349/ent.2023.00047 [Jindex] => 0 [CEmail] => yuya.saito.fwd@gmail.com, [Ris_Time] => 2023-08-22 06:23:05 [Bib_Time] => 2023-08-22 06:23:05 [KeysWordContens] => Retracted: Diffusion magnetic resonance imaging-based surrogate marker in amyotrophic lateral sclerosis, Amyotrophic lateral sclerosis, surrogate marker, diffusion kurtosis imaging, diffusion tensor imaging, free water elimination diffusion tensor imaging, neurite orientation dispersion and density imaging, Amyotrophic lateral sclerosis (ALS) is the most prevalent type of motor neuron disease (MND) and is diagnosed with a delay from the first appearance of symptoms. Surrogate markers that may be used to detect pathological changes before a significant neuronal loss occurs and allow for early intervention with disease-modifying therapy techniques are desperately needed. Using water molecules that diffuse within the tissue and experience displacement on the micron scale, diffusion magnetic resonance imaging (MRI) is a promising technique that can be used to infer microstructural characteristics of the brain, such as microstructural integrity and complexity, axonal density, order, and myelination. Diffusion tensor imaging (DTI) is the primary diffusion MRI technique used to evaluate the pathogenesis of ALS. Neurite orientation dispersion and density imaging (NODDI), diffusion kurtosis imaging (DKI), and free water elimination DTI (FWE-DTI) are only a few of the approaches that have been developed to overcome the shortcomings of the diffusion tensor technique. This article provides a summary of these methods and their potential as surrogate markers for detecting the onset of ALS at an early stage. ,Yuya Saito [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 [AuthorsName] => Yuya Saito ) [47] => Array ( [ArticleId] => 696 [Create_Time] => 2023-08-24 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230829083723.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100446/100446.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100446/100446.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100446/100446_cover.png [JournalsId] => 7 [Title] => Tension pneumocephalus as a complication of surgical evacuation of chronic subdural hematoma: case report and literature review [Abstract] => The management of symptomatic chronic subdural hematoma (CSDH) is surgical evacuation and prognosis in most cases is good. Tension pneumocephalus is the presence of air under pressure in the intracr [AbstractComplete] =>

The management of symptomatic chronic subdural hematoma (CSDH) is surgical evacuation and prognosis in most cases is good. Tension pneumocephalus is the presence of air under pressure in the intracranial cavity. A case of tension pneumocephalus developing as a complication of burr hole evacuation of CSDH is illustrated. In this case, tension pneumocephalus was managed by reopening the wound and saline irrigation with a subdural drain placement. Considering this case report and after a careful review of the literature, the physiopathology, diagnosis, and treatment of this complication are highlighted in the article.

[Names] => Mohammed A. Azab ... Brandon Lucke-Wold [CName] => [Doi] => 10.37349/ent.2023.00046 [Published] => August 23, 2023 [Viewed] => 854 [Downloaded] => 25 [Subject] => Case Report [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00046 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 66 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:177–185 [Recommend] => 0 [Keywords] => Chronic subdural hematoma, tension, pneumocephalus, management [DetailTitle] => Emerging Concepts in Subarachnoid Hemorrhage [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/66 [Id] => 100446 [ris] => https://www.explorationpub.com/uploads/Article/A100446/5f30cc776d6c660124d0d7183185e52c.ris [bib] => https://www.explorationpub.com/uploads/Article/A100446/6573f0f86c420cd3c2c4bd7908a72625.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Azab MA, Hazem A, Lucke-Wold B. Tension pneumocephalus as a complication of surgical evacuation of chronic subdural hematoma: case report and literature review. Explor Neuroprot Ther. 2023;3:177–85. https://doi.org/10.37349/ent.2023.00046 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-08-22 05:09:37 [Bib_Time] => 2023-08-22 05:09:37 [KeysWordContens] => Tension pneumocephalus as a complication of surgical evacuation of chronic subdural hematoma: case report and literature review, Chronic subdural hematoma, tension, pneumocephalus, management, The management of symptomatic chronic subdural hematoma (CSDH) is surgical evacuation and prognosis in most cases is good. Tension pneumocephalus is the presence of air under pressure in the intracranial cavity. A case of tension pneumocephalus developing as a complication of burr hole evacuation of CSDH is illustrated. In this case, tension pneumocephalus was managed by reopening the wound and saline irrigation with a subdural drain placement. Considering this case report and after a careful review of the literature, the physiopathology, diagnosis, and treatment of this complication are highlighted in the article. ,Mohammed A. Azab ... Brandon Lucke-Wold [PublishedText] => Published [IsEdit] => 0 [AccountId] => 83 [Zh] => 1 [AuthorsName] => Mohammed A. Azab, Ahmed Hazem, Brandon Lucke-Wold ) [48] => Array ( [ArticleId] => 702 [Create_Time] => 2023-08-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230828030037.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100449/100449.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100449/100449.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100449/100449_cover.png [JournalsId] => 7 [Title] => Rehabilitation for non-motor symptoms for patients with Parkinson’s disease from an α-synuclein perspective: a narrative review [Abstract] => Parkinson’s disease (PD) is a common neurodegenerative disorder affecting aged population around the world. PD is characterized by neuronal Lewy bodies present in the substantia nigra of the midbr [AbstractComplete] =>

Parkinson’s disease (PD) is a common neurodegenerative disorder affecting aged population around the world. PD is characterized by neuronal Lewy bodies present in the substantia nigra of the midbrain and the loss of dopaminergic neurons with various motor and non-motor symptoms associated with the disease. The protein α-synuclein has been extensively studied for its contribution to PD pathology, as α-synuclein aggregates form the major component of Lewy bodies, a hallmark of PD. In this narrative review, the authors first focus on a brief explanation of α-synuclein aggregation and circumstances under which aggregation can occur, then present a hypothesis for PD pathogenesis in the peripheral nervous system (PNS) and how PD can spread to the central nervous system from the PNS via the transport of α-synuclein aggregates. This article presents arguments both for and against this hypothesis. It also presents various non-pharmacological rehabilitation approaches and management techniques for both motor and non-motor symptoms of PD and the related pathology. This review seeks to examine a possible hypothesis of PD pathogenesis and points to a new research direction focus on rehabilitation therapy for patients with PD. As various non-motor symptoms of PD appear to occur earlier than motor symptoms, more focus on the treatment of non-motor symptoms as well as a better understanding of the biochemical mechanisms behind those non-motor symptoms may lead to better long-term outcomes for patients with PD.

[Names] => Zhaoyang Liu ... Wen Liu [CName] => [Doi] => 10.37349/ent.2023.00049 [Published] => August 27, 2023 [Viewed] => 962 [Downloaded] => 33 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00049 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 122 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:235–257 [Recommend] => 0 [Keywords] => Parkinson’s disease, α-synuclein, non-motor symptoms, rehabilitation [DetailTitle] => Role of the Monoaminergic Systems in the Pathogenesis and the Pathophysiology of Parkinson's Disease [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/122 [Id] => 100449 [ris] => https://www.explorationpub.com/uploads/Article/A100449/88ffb98cda17bff3839c851f128df23b.ris [bib] => https://www.explorationpub.com/uploads/Article/A100449/d11cd6b0762d2c6b745ca94f6baa1a52.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Liu Z, Lemus J, Smirnova IV, Liu W. Rehabilitation for non-motor symptoms for patients with Parkinson’s disease from an α-synuclein perspective: a narrative review. Explor Neuroprot Ther. 2023;3:235–57. https://doi.org/10.37349/ent.2023.00049 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-08-24 01:58:37 [Bib_Time] => 2023-08-24 01:57:02 [KeysWordContens] => Rehabilitation for non-motor symptoms for patients with Parkinson’s disease from an α-synuclein perspective: a narrative review, Parkinson’s disease, α-synuclein, non-motor symptoms, rehabilitation, Parkinson’s disease (PD) is a common neurodegenerative disorder affecting aged population around the world. PD is characterized by neuronal Lewy bodies present in the substantia nigra of the midbrain and the loss of dopaminergic neurons with various motor and non-motor symptoms associated with the disease. The protein α-synuclein has been extensively studied for its contribution to PD pathology, as α-synuclein aggregates form the major component of Lewy bodies, a hallmark of PD. In this narrative review, the authors first focus on a brief explanation of α-synuclein aggregation and circumstances under which aggregation can occur, then present a hypothesis for PD pathogenesis in the peripheral nervous system (PNS) and how PD can spread to the central nervous system from the PNS via the transport of α-synuclein aggregates. This article presents arguments both for and against this hypothesis. It also presents various non-pharmacological rehabilitation approaches and management techniques for both motor and non-motor symptoms of PD and the related pathology. This review seeks to examine a possible hypothesis of PD pathogenesis and points to a new research direction focus on rehabilitation therapy for patients with PD. As various non-motor symptoms of PD appear to occur earlier than motor symptoms, more focus on the treatment of non-motor symptoms as well as a better understanding of the biochemical mechanisms behind those non-motor symptoms may lead to better long-term outcomes for patients with PD. ,Zhaoyang Liu ... Wen Liu [PublishedText] => Published [IsEdit] => 0 [AccountId] => 45 [Zh] => 1 [AuthorsName] => Zhaoyang Liu, Jessica Lemus, Irina V. Smirnova, Wen Liu ) [49] => Array ( [ArticleId] => 848 [Create_Time] => 2023-10-25 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231025084717.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100450/100450.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100450/100450.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100450/100450_cover.png [JournalsId] => 7 [Title] => Cannabinoid CB2 receptor ligands disrupt the sequential regulation of p-MEK1/2 to p-ERK1/2 in mouse brain cortex [Abstract] => Aim The sequential phosphorylation of mitogen-activated protein (MAP) kinases MEK-ERK is the most relevant cellular signaling pathway. This study quantified the parallel in vivo regulation of bra [AbstractComplete] =>

Aim:

The sequential phosphorylation of mitogen-activated protein (MAP) kinases MEK-ERK is the most relevant cellular signaling pathway. This study quantified the parallel in vivo regulation of brain phosphorylation-MEK1/2 (p-MEK1/2) to p-ERK1/2 by mechanistically different cannabinoid 2 (CB2) receptor ligands, i.e., direct (and endogenous) agonists and inverse agonists.

Methods:

Groups of Swiss albino CD1 IGS male adult mice were treated (i.p.) with the CB2 agonist JWH133 (1 mg/kg and 3 mg/kg, 1 h, n = 8) or the CB2 inverse agonist/antagonist AM630 (0.3 mg/kg and 1 mg/kg, 1.5 h, n = 8–9), and 0.9% NaCl (2 mL/kg, 1 h, n = 4–10) as vehicle control. Transgenic male mice overexpressing cortical CB2 receptors [messenger RNA (mRNA) and protein] on a Swiss ICR congenic background (CB2xP) and the corresponding littermates age-matched wild-type (WT) controls were used. Protein forms (total MEK and ERK p-kinases) were resolved by electrophoresis [sodium dodecyl-sulfate polyacrylamide gel electrophoresis (SDS-PAGE) minigels] followed by immunoblotting standard procedures.

Results:

The selective CB2 agonist JWH133 (1 mg/kg and 3 mg/kg, i.p., 1 h) modestly decreased MEK (17%, n = 8) and upregulated ERK (25%, n = 8) activities. The endogenous CB2 agonists (acting on promoted overexpressed receptors) decreased MEK (44%, n = 9) and upregulated ERK (67%, n = 10) activities. The inverse agonist/antagonist AM630 (0.3 mg/kg and 1 mg/kg, i.p., 1.5 h) increases MEK activity (27%, n = 8) without significantly altering that of ERK (5%, n = 9).

Conclusions:

Acute treatments of mice with mechanistically different CB2 receptor ligands (i.e., direct agonists, endogenous agonists, and inverse agonists) resulted in disruption of MEK (p-MEK/total-MEK ratio) to ERK (p-ERK/total-ERK ratio) signals in the brain cortex. This striking disruption of MEK to ERK parallel regulation in the cannabinoid CB2 receptor system in the brain could be relevant to the postulated role of CB2 receptors in various central nervous system (CNS) diseases.

[Names] => Glòria Salort ... Jesús A. García-Sevilla [CName] => [Doi] => 10.37349/ent.2023.00050 [Published] => October 24, 2023 [Viewed] => 713 [Downloaded] => 26 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00050 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 135 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:258–267 [Recommend] => 0 [Keywords] => Cannabinoid 2 receptor, JWH133, cannabinoid 2 receptor overexpression, constitutive cannabinoid 2 receptor activity, cannabinoid 2 inverse agonist/antagonist AM630, MEK-ERK phosphorylation/activation, mouse brain cortex [DetailTitle] => The Urgent Need for New Hypotheses to Develop Effective Therapeutic Tools Against Alzheimer's Disease [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/135 [Id] => 100450 [ris] => https://www.explorationpub.com/uploads/Article/A100450/6cfd677253e5a9874998a3537ac84604.ris [bib] => https://www.explorationpub.com/uploads/Article/A100450/cc5b92d1b749b6918984382b8a7d80a2.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Salort G, Álvaro-Bartolomé M, García-Sevilla JA. Cannabinoid CB2 receptor ligands disrupt the sequential regulation of p-MEK1/2 to p-ERK1/2 in mouse brain cortex. Explor Neuroprot Ther. 2023;3:258–67. https://doi.org/10.37349/ent.2023.00050 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-10-25 08:47:18 [Bib_Time] => 2023-10-25 08:47:18 [KeysWordContens] => Cannabinoid CB2 receptor ligands disrupt the sequential regulation of p-MEK1/2 to p-ERK1/2 in mouse brain cortex, Cannabinoid 2 receptor, JWH133, cannabinoid 2 receptor overexpression, constitutive cannabinoid 2 receptor activity, cannabinoid 2 inverse agonist/antagonist AM630, MEK-ERK phosphorylation/activation, mouse brain cortex, Aim: The sequential phosphorylation of mitogen-activated protein (MAP) kinases MEK-ERK is the most relevant cellular signaling pathway. This study quantified the parallel in vivo regulation of brain phosphorylation-MEK1/2 (p-MEK1/2) to p-ERK1/2 by mechanistically different cannabinoid 2 (CB2) receptor ligands, i.e., direct (and endogenous) agonists and inverse agonists. Methods: Groups of Swiss albino CD1 IGS male adult mice were treated (i.p.) with the CB2 agonist JWH133 (1 mg/kg and 3 mg/kg, 1 h, n = 8) or the CB2 inverse agonist/antagonist AM630 (0.3 mg/kg and 1 mg/kg, 1.5 h, n = 8–9), and 0.9% NaCl (2 mL/kg, 1 h, n = 4–10) as vehicle control. Transgenic male mice overexpressing cortical CB2 receptors [messenger RNA (mRNA) and protein] on a Swiss ICR congenic background (CB2xP) and the corresponding littermates age-matched wild-type (WT) controls were used. Protein forms (total MEK and ERK p-kinases) were resolved by electrophoresis [sodium dodecyl-sulfate polyacrylamide gel electrophoresis (SDS-PAGE) minigels] followed by immunoblotting standard procedures. Results: The selective CB2 agonist JWH133 (1 mg/kg and 3 mg/kg, i.p., 1 h) modestly decreased MEK (17%, n = 8) and upregulated ERK (25%, n = 8) activities. The endogenous CB2 agonists (acting on promoted overexpressed receptors) decreased MEK (44%, n = 9) and upregulated ERK (67%, n = 10) activities. The inverse agonist/antagonist AM630 (0.3 mg/kg and 1 mg/kg, i.p., 1.5 h) increases MEK activity (27%, n = 8) without significantly altering that of ERK (5%, n = 9). Conclusions: Acute treatments of mice with mechanistically different CB2 receptor ligands (i.e., direct agonists, endogenous agonists, and inverse agonists) resulted in disruption of MEK (p-MEK/total-MEK ratio) to ERK (p-ERK/total-ERK ratio) signals in the brain cortex. This striking disruption of MEK to ERK parallel regulation in the cannabinoid CB2 receptor system in the brain could be relevant to the postulated role of CB2 receptors in various central nervous system (CNS) diseases. ,Glòria Salort ... Jesús A. García-Sevilla [PublishedText] => Published [IsEdit] => 0 [AccountId] => 77 [Zh] => 1 [AuthorsName] => Glòria Salort, María Álvaro-Bartolomé, Jesús A. García-Sevilla ) [50] => Array ( [ArticleId] => 854 [Create_Time] => 2023-10-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231025090245.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100451/100451.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100451/100451.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100451/100451_cover.png [JournalsId] => 7 [Title] => Cognitive recovery in psychiatric disorders: transdiagnostic interdisciplinary intervention in a high intensity partial psychiatric in-patient unit [Abstract] => Aim: The present study aims to analyze the impact on cognitive recovery of an interdisciplinary treatment for acute and severe psychiatric patients. Methods: The present research is a natur [AbstractComplete] =>

Aim:

The present study aims to analyze the impact on cognitive recovery of an interdisciplinary treatment for acute and severe psychiatric patients.

Methods:

The present research is a naturalistic observational study of 130 adults (mean age of 47.68 years, 68% women). Clinical severity was assessed using Brief Psychiatry Rating Scale (BPRS), Montgomery-Asberg Depression Rating Scale (MADRS), and Hamilton Anxiety Rating Scale (HARS). Functional performance was evaluated using the Functioning Assessment Short Test (FAST), and cognitive impairment by applying the Montreal Cognitive Assessment (MoCA). Patients were clustered into four diagnostic groups (non-affective psychosis, bipolar, depressive, and personality disorders) and had individualized psychopharmacological treatment. They receive a transdiagnostic group program including several interventions that have shown evidence of beneficial effects over the different cognitive domains impaired in mental illness (attention, speed of processing, memory, working memory, reasoning, and problem-solving), as well as social cognition domains (emotion processing and social skills), in combination with psychoeducation and some strategies oriented to achieve healthy lifestyle routines (balanced diet, physical exercise, sleep hygiene, and smoking and alcohol cessation).

Results:

All clinical scales scores were improved after the end of treatment compared with those achieved at admission (BPRS, MADRS, and HARS scores below the cut-off point for establishing a case diagnosis). MoCA scores improved after the end of treatment concerning admission, both in the total score and in the differentiated cognitive domains, excluding orientation, which remained unchanged in the whole of the sample studied. No statistical significance was found in any comparisons between different diagnostic groups. No correlation between MoCA scores and BPRS, MADRS, or HARS scores at admission or discharge was found.

Conclusions:

These results show that the interdisciplinary therapeutic intervention can be effective for recovering cognitive impairment associated with mental disorders, irrespective of the diagnosis.

[Names] => Ana Isabel De Santiago-Díaz ... Elsa Gómez-Ruiz [CName] => [Doi] => 10.37349/ent.2023.00051 [Published] => October 26, 2023 [Viewed] => 591 [Downloaded] => 16 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00051 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:268–280 [Recommend] => 0 [Keywords] => Cognitive impairment, cognitive recovery, cognition, psychiatric disorder, transdiagnostic, clinical interventions [DetailTitle] => [DetailUrl] => [Id] => 100451 [ris] => https://www.explorationpub.com/uploads/Article/A100451/6bf9f3a940bd78080953f4024be3e39b.ris [bib] => https://www.explorationpub.com/uploads/Article/A100451/d243442a727c136218cb461ced6879fd.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => De Santiago-Díaz AI, Pérez-Poo T, Pindado-Jiménez E, Cortez-Astudillo G, Zabala-Alonso A, Gómez-Ruiz E. Cognitive recovery in psychiatric disorders: transdiagnostic interdisciplinary intervention in a high intensity partial psychiatric in-patient unit. Explor Neuroprot Ther. 2023;3:268–80. https://doi.org/10.37349/ent.2023.00051 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-10-18 07:18:45 [Bib_Time] => 2023-10-18 07:18:45 [KeysWordContens] => Cognitive recovery in psychiatric disorders: transdiagnostic interdisciplinary intervention in a high intensity partial psychiatric in-patient unit, Cognitive impairment, cognitive recovery, cognition, psychiatric disorder, transdiagnostic, clinical interventions, Aim: The present study aims to analyze the impact on cognitive recovery of an interdisciplinary treatment for acute and severe psychiatric patients. Methods: The present research is a naturalistic observational study of 130 adults (mean age of 47.68 years, 68% women). Clinical severity was assessed using Brief Psychiatry Rating Scale (BPRS), Montgomery-Asberg Depression Rating Scale (MADRS), and Hamilton Anxiety Rating Scale (HARS). Functional performance was evaluated using the Functioning Assessment Short Test (FAST), and cognitive impairment by applying the Montreal Cognitive Assessment (MoCA). Patients were clustered into four diagnostic groups (non-affective psychosis, bipolar, depressive, and personality disorders) and had individualized psychopharmacological treatment. They receive a transdiagnostic group program including several interventions that have shown evidence of beneficial effects over the different cognitive domains impaired in mental illness (attention, speed of processing, memory, working memory, reasoning, and problem-solving), as well as social cognition domains (emotion processing and social skills), in combination with psychoeducation and some strategies oriented to achieve healthy lifestyle routines (balanced diet, physical exercise, sleep hygiene, and smoking and alcohol cessation). Results: All clinical scales scores were improved after the end of treatment compared with those achieved at admission (BPRS, MADRS, and HARS scores below the cut-off point for establishing a case diagnosis). MoCA scores improved after the end of treatment concerning admission, both in the total score and in the differentiated cognitive domains, excluding orientation, which remained unchanged in the whole of the sample studied. No statistical significance was found in any comparisons between different diagnostic groups. No correlation between MoCA scores and BPRS, MADRS, or HARS scores at admission or discharge was found. Conclusions: These results show that the interdisciplinary therapeutic intervention can be effective for recovering cognitive impairment associated with mental disorders, irrespective of the diagnosis. ,Ana Isabel De Santiago-Díaz ... Elsa Gómez-Ruiz [PublishedText] => Published [IsEdit] => 0 [AccountId] => 78 [Zh] => 1 [AuthorsName] => Ana Isabel De Santiago-Díaz, Teresa Pérez-Poo, Erika Pindado-Jiménez, Gabriela Cortez-Astudillo, Aranzazu Zabala-Alonso, Elsa Gómez-Ruiz ) [51] => Array ( [ArticleId] => 862 [Create_Time] => 2023-10-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231026051440.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100452/100452.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100452/100452.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100452/100452_cover.png [JournalsId] => 7 [Title] => The effects of post-translational modifications on alpha-synuclein aggregation and immune cell activation in Parkinson’s disease [Abstract] => Post-translational modifications (PTMs) of alpha-synuclein (α-syn) can alter protein aggregation propensity to affect α-syn oligomer and fibril formation. The inflammatory response in Parkinson’ [AbstractComplete] =>

Post-translational modifications (PTMs) of alpha-synuclein (α-syn) can alter protein aggregation propensity to affect α-syn oligomer and fibril formation. The inflammatory response in Parkinson’s disease (PD) is mediated by microglia, astrocytes, T cells, B cells, macrophages, and neutrophils, which respond to α-syn aggregates in an attempt to clear synucleinopathy and restore brain homeostasis. This review focuses on the effects of PTMs on α-syn aggregation and cell-specific immune responses to α-syn aggregates in the context of PD.

[Names] => Zaina Khan, Yoo Jin Jung [CName] => [Doi] => 10.37349/ent.2023.00052 [Published] => October 26, 2023 [Viewed] => 783 [Downloaded] => 21 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00052 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 118 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:281–298 [Recommend] => 0 [Keywords] => Alpha-synuclein, Parkinson’s disease, neuroimmunology, post-translational modifications, protein aggregation [DetailTitle] => Parkinson’s Disease: Principal Targets and Interventional Mechanisms [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/118 [Id] => 100452 [ris] => https://www.explorationpub.com/uploads/Article/A100452/c17b0c4c97891d49554a19ba912f65a5.ris [bib] => https://www.explorationpub.com/uploads/Article/A100452/b6199d6d5e0bfb38978ac0d817b02386.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Khan Z, Jung YJ. The effects of post-translational modifications on alpha-synuclein aggregation and immune cell activation in Parkinson’s disease. Explor Neuroprot Ther. 2023;3:281–98. https://doi.org/10.37349/ent.2023.00052 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-10-24 02:48:34 [Bib_Time] => 2023-10-24 02:48:34 [KeysWordContens] => The effects of post-translational modifications on alpha-synuclein aggregation and immune cell activation in Parkinson’s disease, Alpha-synuclein, Parkinson’s disease, neuroimmunology, post-translational modifications, protein aggregation, Post-translational modifications (PTMs) of alpha-synuclein (α-syn) can alter protein aggregation propensity to affect α-syn oligomer and fibril formation. The inflammatory response in Parkinson’s disease (PD) is mediated by microglia, astrocytes, T cells, B cells, macrophages, and neutrophils, which respond to α-syn aggregates in an attempt to clear synucleinopathy and restore brain homeostasis. This review focuses on the effects of PTMs on α-syn aggregation and cell-specific immune responses to α-syn aggregates in the context of PD. ,Zaina Khan, Yoo Jin Jung [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 1 [AuthorsName] => Zaina Khan, Yoo Jin Jung ) [52] => Array ( [ArticleId] => 882 [Create_Time] => 2023-10-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202311/20231101011146.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100453/100453.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100453/100453.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100453/cover.png [JournalsId] => 7 [Title] => Aldh1a1 and additional markers of dopamine cell heterogeneity in substantia nigra and ventral tegmental area identified as preserved in two transgenic α-synuclein mouse models of neurodegenerative disease [Abstract] => Aim: Parkinson’s disease (PD) is characterized by degeneration of midbrain dopamine neurons and synucleinopathy [aggregated alpha-synuclein protein (αSyn)]. The correlation between αSyn patho [AbstractComplete] =>

Aim:

Parkinson’s disease (PD) is characterized by degeneration of midbrain dopamine neurons and synucleinopathy [aggregated alpha-synuclein protein (αSyn)]. The correlation between αSyn pathology and dopamine neuron degeneration remains to be fully established. Mouse models of PD are commonly used to increase knowledge of disease mechanisms. Lately, midbrain dopamine neurons have gained attention as more heterogeneous than previously recognized. With the aim to determine how the midbrain dopamine system in mice is affected in the presence of αSyn pathology, this brain system was studied in two transgenic mouse models of synucleinopathy.

Methods:

Brain sections from two previously described transgenic mouse lines verified for αSyn pathology through expression of the human αSyn gene (SNCA) under control of the Thy-1 promoter [Thy1-h[A30P]αSyn and Thy1-h[wt]αSyn (L61)], were analyzed using fluorescent in situ hybridization (FISH) and compared with matching sections from wild-type control mice. Probes directed towards mouse and human αSyn mRNA, and a battery of probes towards mRNAs representative of dopamine cell identity and heterogeneity, were implemented.

Results:

First, validation of αSyn-encoding mRNA was performed. Ample ectopic αSyn mRNA was observed throughout the brain of mice of each transgenic line. Next, midbrain dopamine neurons located in substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) were analyzed using a battery of general and subpopulation-specific dopamine cell markers. This included tyrosine hydroxylase (Th), vesicular monoamine transporter 2 (Vmat2), dopamine transporter (Dat), aldehyde dehydrogenase 1 family member A1 (Aldh1a1), G-protein-activated inward-rectifying potassium channel type 2 (Girk2), calbindin 1 (Calb1), Calb2, gastrin-releasing peptide (Grp), and vesicular glutamate transporter 2 (Vglut2) mRNAs. No difference between transgenic and control mice was observed for any analyzed marker in either the Thy1-h[A30P]αSyn or Thy1-h[wt]αSyn transgenic mouse line.

Conclusions:

This study demonstrates remarkable robustness of midbrain dopamine cell integrity in the presence of brain-wide ectopic human αSyn in two transgenic mouse models of neurodegenerative disease, motivating further study into mechanisms correlating synucleinopathy with dopamine neuron degeneration in rodent models relevant to PD.

[Names] => Bianca Vlcek ... Åsa Wallén-Mackenzie [CName] => [Doi] => 10.37349/ent.2023.00053 [Published] => October 30, 2023 [Viewed] => 1176 [Downloaded] => 24 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00053 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 122 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:299–327 [Recommend] => 0 [Keywords] => Aldehyde dehydrogenase, alpha-synuclein, Parkinson’s disease, SNCA, transgenic mice, vesicular monoamine transporter 2, substantia nigra pars compacta, ventral tegmental area [DetailTitle] => Role of the Monoaminergic Systems in the Pathogenesis and the Pathophysiology of Parkinsons Disease [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/122 [Id] => 100453 [ris] => https://www.explorationpub.com/uploads/Article/A100453/d51764e96d572063f08cff2c7894c646.ris [bib] => https://www.explorationpub.com/uploads/Article/A100453/2e0740cd9057e9cd5ca8dd354112ea36.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Vlcek B, Dumas S, Ekmark-Lewén S, Rubino E, Ingelsson M, Wallén-Mackenzie Å. Aldh1a1 and additional markers of dopamine cell heterogeneity in substantia nigra and ventral tegmental area identified as preserved in two transgenic α-synuclein mouse models of neurodegenerative disease. Explor Neuroprot Ther. 2023;3:299–327. https://doi.org/10.37349/ent.2023.00053 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-11-01 01:11:48 [Bib_Time] => 2023-11-01 01:11:48 [KeysWordContens] => Aldh1a1 and additional markers of dopamine cell heterogeneity in substantia nigra and ventral tegmental area identified as preserved in two transgenic α-synuclein mouse models of neurodegenerative disease, Aldehyde dehydrogenase, alpha-synuclein, Parkinson’s disease, SNCA, transgenic mice, vesicular monoamine transporter 2, substantia nigra pars compacta, ventral tegmental area, Aim: Parkinson’s disease (PD) is characterized by degeneration of midbrain dopamine neurons and synucleinopathy [aggregated alpha-synuclein protein (αSyn)]. The correlation between αSyn pathology and dopamine neuron degeneration remains to be fully established. Mouse models of PD are commonly used to increase knowledge of disease mechanisms. Lately, midbrain dopamine neurons have gained attention as more heterogeneous than previously recognized. With the aim to determine how the midbrain dopamine system in mice is affected in the presence of αSyn pathology, this brain system was studied in two transgenic mouse models of synucleinopathy. Methods: Brain sections from two previously described transgenic mouse lines verified for αSyn pathology through expression of the human αSyn gene (SNCA) under control of the Thy-1 promoter [Thy1-h[A30P]αSyn and Thy1-h[wt]αSyn (L61)], were analyzed using fluorescent in situ hybridization (FISH) and compared with matching sections from wild-type control mice. Probes directed towards mouse and human αSyn mRNA, and a battery of probes towards mRNAs representative of dopamine cell identity and heterogeneity, were implemented. Results: First, validation of αSyn-encoding mRNA was performed. Ample ectopic αSyn mRNA was observed throughout the brain of mice of each transgenic line. Next, midbrain dopamine neurons located in substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) were analyzed using a battery of general and subpopulation-specific dopamine cell markers. This included tyrosine hydroxylase (Th), vesicular monoamine transporter 2 (Vmat2), dopamine transporter (Dat), aldehyde dehydrogenase 1 family member A1 (Aldh1a1), G-protein-activated inward-rectifying potassium channel type 2 (Girk2), calbindin 1 (Calb1), Calb2, gastrin-releasing peptide (Grp), and vesicular glutamate transporter 2 (Vglut2) mRNAs. No difference between transgenic and control mice was observed for any analyzed marker in either the Thy1-h[A30P]αSyn or Thy1-h[wt]αSyn transgenic mouse line. Conclusions: This study demonstrates remarkable robustness of midbrain dopamine cell integrity in the presence of brain-wide ectopic human αSyn in two transgenic mouse models of neurodegenerative disease, motivating further study into mechanisms correlating synucleinopathy with dopamine neuron degeneration in rodent models relevant to PD. ,Bianca Vlcek ... Åsa Wallén-Mackenzie [PublishedText] => Published [IsEdit] => 0 [AccountId] => 79 [Zh] => 1 [AuthorsName] => Bianca Vlcek, Sylvie Dumas, Sara Ekmark-Lewén, Eleonora Rubino, Martin Ingelsson, Åsa Wallén-Mackenzie ) [53] => Array ( [ArticleId] => 902 [Create_Time] => 2023-10-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231030020036.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100454/100454.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100454/100454.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100454/100454_cover.png [JournalsId] => 7 [Title] => Neuroprotective astroglial response to neural damage and its relevance to affective disorders [Abstract] => Astrocytes not only support neuronal function with essential roles in synaptic neurotransmission, action potential propagation, metabolic support, or neuroplastic and developmental adaptations. They [AbstractComplete] =>

Astrocytes not only support neuronal function with essential roles in synaptic neurotransmission, action potential propagation, metabolic support, or neuroplastic and developmental adaptations. They also respond to damage or dysfunction in surrounding neurons and oligodendrocytes by releasing neurotrophic factors and other molecules that increase the survival of the supported cells or contribute to mechanisms of structural and molecular restoration. The neuroprotective responsiveness of astrocytes is based on their ability to sense signals of degeneration, metabolic jeopardy, and structural damage, and on their aptitude to locally deliver specific molecules to remedy threats to the molecular and structural features of their cellular partners. To the extent that neuronal and other glial cell disturbances are known to occur in affective disorders, astrocyte responsiveness to those disturbances may help to better understand the roles astrocytes play in affective disorders. The astrocytic sensing apparatus supporting those responses involves receptors for neurotransmitters, purines, cell adhesion molecules, and growth factors. Astrocytes also share with the immune system the capacity to respond to cytokines released upon neuronal damage. In addition, in response to specific signals, astrocytes release unique factors such as clusterin or humanin that have been shown to exert potent neuroprotective effects. Astrocytes integrate the signals above to further deliver structural lipids, remove toxic metabolites, stabilize the osmotic environment, normalize neurotransmitters, provide antioxidant protection, facilitate synaptogenesis, and act as barriers to contain varied deleterious signals, some of which have been described in brain regions relevant to affective disorders and related animal models. Since various injurious signals that activate astrocytes have been implicated in different aspects of the etiopathology of affective disorders, particularly in relation to the diagnosis of depression, potentiating the corresponding astrocyte neuroprotective responses may provide additional opportunities to improve or complement available pharmacological and behavioral therapies for affective disorders.

[Names] => José Javier Miguel-Hidalgo [CName] => [Doi] => 10.37349/ent.2023.00054 [Published] => October 31, 2023 [Viewed] => 817 [Downloaded] => 19 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00054 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 74 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:328–345 [Recommend] => 0 [Keywords] => Astrocytes, neuroprotection, glutamatergic, neurotrophins, synaptic, antioxidant, oligodendrocytes [DetailTitle] => Glia and Neuroprotection [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/74 [Id] => 100454 [ris] => https://www.explorationpub.com/uploads/Article/A100454/fa703064ee61518351902af61446407b.ris [bib] => https://www.explorationpub.com/uploads/Article/A100454/22389f740e47fe276063ca3608e905b2.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Miguel-Hidalgo JJ. Neuroprotective astroglial response to neural damage and its relevance to affective disorders. Explor Neuroprot Ther. 2023;3:328–45. https://doi.org/10.37349/ent.2023.00054 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-10-27 07:05:21 [Bib_Time] => 2023-10-27 07:05:21 [KeysWordContens] => Neuroprotective astroglial response to neural damage and its relevance to affective disorders, Astrocytes, neuroprotection, glutamatergic, neurotrophins, synaptic, antioxidant, oligodendrocytes, Astrocytes not only support neuronal function with essential roles in synaptic neurotransmission, action potential propagation, metabolic support, or neuroplastic and developmental adaptations. They also respond to damage or dysfunction in surrounding neurons and oligodendrocytes by releasing neurotrophic factors and other molecules that increase the survival of the supported cells or contribute to mechanisms of structural and molecular restoration. The neuroprotective responsiveness of astrocytes is based on their ability to sense signals of degeneration, metabolic jeopardy, and structural damage, and on their aptitude to locally deliver specific molecules to remedy threats to the molecular and structural features of their cellular partners. To the extent that neuronal and other glial cell disturbances are known to occur in affective disorders, astrocyte responsiveness to those disturbances may help to better understand the roles astrocytes play in affective disorders. The astrocytic sensing apparatus supporting those responses involves receptors for neurotransmitters, purines, cell adhesion molecules, and growth factors. Astrocytes also share with the immune system the capacity to respond to cytokines released upon neuronal damage. In addition, in response to specific signals, astrocytes release unique factors such as clusterin or humanin that have been shown to exert potent neuroprotective effects. Astrocytes integrate the signals above to further deliver structural lipids, remove toxic metabolites, stabilize the osmotic environment, normalize neurotransmitters, provide antioxidant protection, facilitate synaptogenesis, and act as barriers to contain varied deleterious signals, some of which have been described in brain regions relevant to affective disorders and related animal models. Since various injurious signals that activate astrocytes have been implicated in different aspects of the etiopathology of affective disorders, particularly in relation to the diagnosis of depression, potentiating the corresponding astrocyte neuroprotective responses may provide additional opportunities to improve or complement available pharmacological and behavioral therapies for affective disorders. ,José Javier Miguel-Hidalgo [PublishedText] => Published [IsEdit] => 0 [AccountId] => 78 [Zh] => 1 [AuthorsName] => José Javier Miguel-Hidalgo ) [54] => Array ( [ArticleId] => 916 [Create_Time] => 2023-10-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231031061044.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100455/100455.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100455/100455.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100455/100455-cover.png [JournalsId] => 7 [Title] => Stem cell therapy in neurological disorders: promises and concerns [Abstract] => Self-neuronal regeneration is often limited or nonexistent after neuronal cell damage, making new technologies necessary for treating neurological damage. Although the brain can partially compensate [AbstractComplete] =>

Self-neuronal regeneration is often limited or nonexistent after neuronal cell damage, making new technologies necessary for treating neurological damage. Although the brain can partially compensate by increasing its plasticity, these compensatory mechanisms can never fully restore the pre-damage state. Analysis of the literature regarding stem cell therapy in case of neurological disorders. Stem cells have shown promise for treating various neurological disorders and disabilities due to their regenerative capacity. Transplanting or administration of different types of stem cells has yielded promising results in animal models and early clinical trials. However, concerns remain regarding their implementation. The type of stem cell used, the optimal method and route of administration, the number of stem cells administered, preconditioning, and the injection schedule all need to be determined. Additionally, the long-term safety of stem cell treatment and the recipient’s age requires further investigation. Despite these concerns, stem cell therapy holds tremendous promise for treating neurological disorders, and continued research and well-designed studies will be crucial for unlocking its full potential.

[Names] => Said Hachimi-Idrissi [CName] => [Doi] => 10.37349/ent.2023.00055 [Published] => October 31, 2023 [Viewed] => 599 [Downloaded] => 13 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00055 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 162 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:346–362 [Recommend] => 0 [Keywords] => Neural stem cells, embryonic stem cells, induced pluripotent stem cells, adult mesenchymal stem, quantity, route of administration, graphene, neurological disorders [DetailTitle] => Therapeutic Targets for Neuroprotection in Ischemic Stroke [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/162 [Id] => 100455 [ris] => https://www.explorationpub.com/uploads/Article/A100455/f18f12c60c250e2b322e70f34b7ff238.ris [bib] => https://www.explorationpub.com/uploads/Article/A100455/a34ae48ff1d248a53d9f487f9d80bc77.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Hachimi-Idrissi S. Stem cell therapy in neurological disorders: promises and concerns. Explor Neuroprot Ther. 2023;3:346–62. https://doi.org/10.37349/ent.2023.00055 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-10-30 09:44:43 [Bib_Time] => 2023-10-30 09:44:43 [KeysWordContens] => Stem cell therapy in neurological disorders: promises and concerns, Neural stem cells, embryonic stem cells, induced pluripotent stem cells, adult mesenchymal stem, quantity, route of administration, graphene, neurological disorders, Self-neuronal regeneration is often limited or nonexistent after neuronal cell damage, making new technologies necessary for treating neurological damage. Although the brain can partially compensate by increasing its plasticity, these compensatory mechanisms can never fully restore the pre-damage state. Analysis of the literature regarding stem cell therapy in case of neurological disorders. Stem cells have shown promise for treating various neurological disorders and disabilities due to their regenerative capacity. Transplanting or administration of different types of stem cells has yielded promising results in animal models and early clinical trials. However, concerns remain regarding their implementation. The type of stem cell used, the optimal method and route of administration, the number of stem cells administered, preconditioning, and the injection schedule all need to be determined. Additionally, the long-term safety of stem cell treatment and the recipient’s age requires further investigation. Despite these concerns, stem cell therapy holds tremendous promise for treating neurological disorders, and continued research and well-designed studies will be crucial for unlocking its full potential. ,Said Hachimi-Idrissi [PublishedText] => Published [IsEdit] => 0 [AccountId] => 78 [Zh] => 1 [AuthorsName] => Said Hachimi-Idrissi ) [55] => Array ( [ArticleId] => 917 [Create_Time] => 2023-10-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231031075511.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100456/100456.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100456/100456.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100456/100456_cover.png [JournalsId] => 7 [Title] => Exploration of transcutaneous vagus nerve stimulation as a treatment option for adjuvant cancer and heart failure therapy [Abstract] => Vagus nerve stimulation (VNS) has gained prominence in the treatment of various clinical disorders such as migraine, depression, and tinnitus. Based on increased scientific knowledge of the VNS and [AbstractComplete] =>

Vagus nerve stimulation (VNS) has gained prominence in the treatment of various clinical disorders such as migraine, depression, and tinnitus. Based on increased scientific knowledge of the VNS and insights into the vagus nerve (VN) function and anatomy/conduction, robust treatment approaches have been developed. There are both noninvasive and invasive VNS (iVNS) techniques. Currently, only iVNS techniques are approved by the US Food and Drug Administration (FDA). In contrast, transcutaneous VNS (tVNS) is a new treatment option that is receiving increasing attention. The tVNS application uses the cutaneous distribution of afferent VN fibers in the auricle, the auricular branch of the VN (ABVN), or in the neck, the cervical branch of the VN (CBVN). However, the tVNS technique has not yet been sufficiently researched in its application and mode of action to be used clinically on a large scale. Moreover, the stimulation parameters of the VN vary widely in different studies. Despite the growing number of research papers on this topic, more coherence in neurostimulation research and neuroanatomical basis is needed. The aim of this review is to highlight new clinical treatment options based on existing clinically applied treatment options. In this article, current clinical applications of tVNS are analyzed and important stimulation parameters are highlighted. Based on this data, useful new tVNS therapies are recommended. The focus will be placed on the study of inflammatory processes associated with cancer and on applications to cardiovascular events such as heart failure.

[Names] => Niklas Frank ... Carola Y. Förster [CName] => [Doi] => 10.37349/ent.2023.00056 [Published] => October 31, 2023 [Viewed] => 1139 [Downloaded] => 34 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00056 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 55 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:363–397 [Recommend] => 0 [Keywords] => Vagus nerve, transcutaneous vagus nerve stimulation, inflammation, cancer, heart failure with preserved ejection fraction [DetailTitle] => Intervention of Neuroimmune Responses [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/55 [Id] => 100456 [ris] => https://www.explorationpub.com/uploads/Article/A100456/301c4a3d85afc0263073b9e4953f1505.ris [bib] => https://www.explorationpub.com/uploads/Article/A100456/1ff69952bb127b71291786935310858d.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Frank N, Nagai M, Förster CY. Exploration of transcutaneous vagus nerve stimulation as a treatment option for adjuvant cancer and heart failure therapy. Explor Neuroprot Ther. 2023;3:363–97. https://doi.org/10.37349/ent.2023.00056 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-10-31 05:48:56 [Bib_Time] => 2023-10-31 05:48:56 [KeysWordContens] => Exploration of transcutaneous vagus nerve stimulation as a treatment option for adjuvant cancer and heart failure therapy, Vagus nerve, transcutaneous vagus nerve stimulation, inflammation, cancer, heart failure with preserved ejection fraction, Vagus nerve stimulation (VNS) has gained prominence in the treatment of various clinical disorders such as migraine, depression, and tinnitus. Based on increased scientific knowledge of the VNS and insights into the vagus nerve (VN) function and anatomy/conduction, robust treatment approaches have been developed. There are both noninvasive and invasive VNS (iVNS) techniques. Currently, only iVNS techniques are approved by the US Food and Drug Administration (FDA). In contrast, transcutaneous VNS (tVNS) is a new treatment option that is receiving increasing attention. The tVNS application uses the cutaneous distribution of afferent VN fibers in the auricle, the auricular branch of the VN (ABVN), or in the neck, the cervical branch of the VN (CBVN). However, the tVNS technique has not yet been sufficiently researched in its application and mode of action to be used clinically on a large scale. Moreover, the stimulation parameters of the VN vary widely in different studies. Despite the growing number of research papers on this topic, more coherence in neurostimulation research and neuroanatomical basis is needed. The aim of this review is to highlight new clinical treatment options based on existing clinically applied treatment options. In this article, current clinical applications of tVNS are analyzed and important stimulation parameters are highlighted. Based on this data, useful new tVNS therapies are recommended. The focus will be placed on the study of inflammatory processes associated with cancer and on applications to cardiovascular events such as heart failure. ,Niklas Frank ... Carola Y. Förster [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 1 [AuthorsName] => Niklas Frank, Michiaki Nagai, Carola Y. Förster ) [56] => Array ( [ArticleId] => 929 [Create_Time] => 2023-11-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202311/20231101033314.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100457/100457.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100457/100457.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100457/100457_cover.png [JournalsId] => 7 [Title] => Efficacy and safety of CDP-choline, cerebrolysin, MLC601, and edaravone in recovery of patients with acute ischemic strokes: a meta-analysis [Abstract] => Aim: Stroke is the second most common cause of mortality and disability worldwide with ischemic strokes being the predominant type. The advent of neuroprotectants brought hope of improved outcome [AbstractComplete] =>

Aim:

Stroke is the second most common cause of mortality and disability worldwide with ischemic strokes being the predominant type. The advent of neuroprotectants brought hope of improved outcomes and quality of life, but current guidelines, despite numerous trials, have no strong recommendation advising their use. This meta-analysis aims to evaluate the degree of effect and safety of the neuroprotectants cytidine-5’-diphosphocholine (CDP-choline), cerebrolysin, edaravone, and MLC601, in the recovery of patients with cerebral infarcts.

Methods:

An extensive literature search, through the databases of PubMed, PMC, Cochrane, and Ovid, was done with the keywords “CDP-choline”, “cerebrolysin”, “MLC601”, and “edaravone” each combined with the term “acute ischemic stroke”. Eligible studies included randomized controlled trials of these neuroprotectants administered to patients with acute ischemic strokes. A total of 2,025 studies were found, and after the application of screening criteria, 24 studies were eligible for analysis.

Results:

The analysis showed that the functional outcome of patients with acute ischemic strokes improved significantly when receiving neuroprotectants versus placebo supported by an odds ratio = 0.29 (0.09–0.50) with a confidence interval of 95%. The P-values are 0.0022 for the one-tailed test, and 0.0030 for the two-tailed test which express the significant improvement of functional outcomes in patients with acute ischemic strokes taking neuroprotectants.

Conclusions:

This study thus supports the use of neuroprotectants in patients with acute ischemic strokes to improve long-term functional outcomes and ultimately quality of life.

[Names] => Shafiq Dexter B. Abou Zaki, Johnny K. Lokin [CName] => [Doi] => 10.37349/ent.2023.00057 [Published] => October 31, 2023 [Viewed] => 813 [Downloaded] => 17 [Subject] => Meta-Analysis [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00057 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 162 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:398–408 [Recommend] => 0 [Keywords] => Ischemic stroke, neuroprotectants, CDP-choline, cerebrolysin, edaravone, MLC601 [DetailTitle] => Therapeutic Targets for Neuroprotection in Ischemic Stroke [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/162 [Id] => 100457 [ris] => https://www.explorationpub.com/uploads/Article/A100457/0eef239130b5366175d052295e96447c.ris [bib] => https://www.explorationpub.com/uploads/Article/A100457/b9f8cdd2c0686e2e199d1bcd90b26cae.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Abou Zaki SDB, Lokin JK. Efficacy and safety of CDP-choline, cerebrolysin, MLC601, and edaravone in recovery of patients with acute ischemic strokes: a meta-analysis. Explor Neuroprot Ther. 2023;3:398–408. https://doi.org/10.37349/ent.2023.00057 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-10-31 10:50:13 [Bib_Time] => 2023-11-01 03:26:15 [KeysWordContens] => Efficacy and safety of CDP-choline, cerebrolysin, MLC601, and edaravone in recovery of patients with acute ischemic strokes: a meta-analysis, Ischemic stroke, neuroprotectants, CDP-choline, cerebrolysin, edaravone, MLC601, Aim: Stroke is the second most common cause of mortality and disability worldwide with ischemic strokes being the predominant type. The advent of neuroprotectants brought hope of improved outcomes and quality of life, but current guidelines, despite numerous trials, have no strong recommendation advising their use. This meta-analysis aims to evaluate the degree of effect and safety of the neuroprotectants cytidine-5’-diphosphocholine (CDP-choline), cerebrolysin, edaravone, and MLC601, in the recovery of patients with cerebral infarcts. Methods: An extensive literature search, through the databases of PubMed, PMC, Cochrane, and Ovid, was done with the keywords “CDP-choline”, “cerebrolysin”, “MLC601”, and “edaravone” each combined with the term “acute ischemic stroke”. Eligible studies included randomized controlled trials of these neuroprotectants administered to patients with acute ischemic strokes. A total of 2,025 studies were found, and after the application of screening criteria, 24 studies were eligible for analysis. Results: The analysis showed that the functional outcome of patients with acute ischemic strokes improved significantly when receiving neuroprotectants versus placebo supported by an odds ratio = 0.29 (0.09–0.50) with a confidence interval of 95%. The P-values are 0.0022 for the one-tailed test, and 0.0030 for the two-tailed test which express the significant improvement of functional outcomes in patients with acute ischemic strokes taking neuroprotectants. Conclusions: This study thus supports the use of neuroprotectants in patients with acute ischemic strokes to improve long-term functional outcomes and ultimately quality of life. ,Shafiq Dexter B. Abou Zaki, Johnny K. Lokin [PublishedText] => Published [IsEdit] => 0 [AccountId] => 21 [Zh] => 1 [AuthorsName] => Shafiq Dexter B. Abou Zaki, Johnny K. Lokin ) [57] => Array ( [ArticleId] => 940 [Create_Time] => 2023-11-17 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240220062926.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100458/100458.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100458/100458.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100458/100458-cover.png [JournalsId] => 7 [Title] => From the ocean to the brain: harnessing the power of marine algae for neuroprotection and therapeutic advances [Abstract] => Recent investigations have shed light on the potential of seaweed, an abundant source of bioactive compounds, to mitigate and combat neurodegenerative diseases. In this comprehensive review, the acc [AbstractComplete] =>

Recent investigations have shed light on the potential of seaweed, an abundant source of bioactive compounds, to mitigate and combat neurodegenerative diseases. In this comprehensive review, the accumulating evidence supporting the neuroprotective properties of seaweed-derived compounds is evaluated and their putative mechanisms of action are elucidated. The background of this review encompasses the general understanding of neurodegenerative diseases as debilitating conditions characterized by the progressive loss of nerve cell function and viability in the central nervous system. Furthermore, the global prevalence of these diseases, encompassing Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease, and the persistent absence of effective treatments are emphasized. To address this critical issue, an innovative avenue of research is explored by investigating the potential of seaweed and its diverse array of bioactive compounds. By examining the available literature, the evidence supporting the neuroprotective effects of seaweed-derived compounds is consolidated. These bioactive constituents exhibit promising properties in preventing and mitigating neurodegeneration. Mechanistically, their actions involve intricate pathways that contribute to neuronal survival, reduction of oxidative stress, inhibition of neuroinflammation, and modulation of protein aggregation processes. This review provides a comprehensive analysis of the mechanisms underlying the neuroprotective effects of seaweed compounds. In conclusion, this review highlights the potential of seaweed as a valuable source of neuroprotective compounds and underscores the advancements made in this burgeoning field. The identification and elucidation of the mechanisms through which seaweed compounds exert their neuroprotective effects hold promise for the development of novel therapeutic interventions. These findings transcend disciplinary boundaries, offering insight into the potential application of seaweed-derived compounds as a valuable resource for combating neurodegenerative diseases across scientific domains.

[Names] => Leonel Pereira, Ana Valado [CName] => LeonelPereira, [Doi] => 10.37349/ent.2023.00058 [Published] => November 17, 2023 [Viewed] => 2473 [Downloaded] => 59 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00058 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 144 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:409–428 [Recommend] => 0 [Keywords] => Neuroprotectant, neurodegenerative diseases, plant-derived compounds, polysaccharides, carotenoids, antioxidants, anti-inflammatory agents [DetailTitle] => Natural Products in Neurotherapeutic Applications [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/144 [Id] => 100458 [ris] => https://www.explorationpub.com/uploads/Article/A100458/0674bb64131fa19b8c4afcfd3f396193.ris [bib] => https://www.explorationpub.com/uploads/Article/A100458/3fe1586e921cee9a63310589cb1929bc.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-05-27 [CitethisArticle] => Pereira L, Valado A. From the ocean to the brain: harnessing the power of marine algae for neuroprotection and therapeutic advances. Explor Neuroprot Ther. 2023;3:409–28. https://doi.org/10.37349/ent.2023.00058 [Jindex] => 0 [CEmail] => leonel.pereira@uc.pt, [Ris_Time] => 2023-11-15 03:39:34 [Bib_Time] => 2023-11-15 03:39:34 [KeysWordContens] => From the ocean to the brain: harnessing the power of marine algae for neuroprotection and therapeutic advances, Neuroprotectant, neurodegenerative diseases, plant-derived compounds, polysaccharides, carotenoids, antioxidants, anti-inflammatory agents, Recent investigations have shed light on the potential of seaweed, an abundant source of bioactive compounds, to mitigate and combat neurodegenerative diseases. In this comprehensive review, the accumulating evidence supporting the neuroprotective properties of seaweed-derived compounds is evaluated and their putative mechanisms of action are elucidated. The background of this review encompasses the general understanding of neurodegenerative diseases as debilitating conditions characterized by the progressive loss of nerve cell function and viability in the central nervous system. Furthermore, the global prevalence of these diseases, encompassing Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease, and the persistent absence of effective treatments are emphasized. To address this critical issue, an innovative avenue of research is explored by investigating the potential of seaweed and its diverse array of bioactive compounds. By examining the available literature, the evidence supporting the neuroprotective effects of seaweed-derived compounds is consolidated. These bioactive constituents exhibit promising properties in preventing and mitigating neurodegeneration. Mechanistically, their actions involve intricate pathways that contribute to neuronal survival, reduction of oxidative stress, inhibition of neuroinflammation, and modulation of protein aggregation processes. This review provides a comprehensive analysis of the mechanisms underlying the neuroprotective effects of seaweed compounds. In conclusion, this review highlights the potential of seaweed as a valuable source of neuroprotective compounds and underscores the advancements made in this burgeoning field. The identification and elucidation of the mechanisms through which seaweed compounds exert their neuroprotective effects hold promise for the development of novel therapeutic interventions. These findings transcend disciplinary boundaries, offering insight into the potential application of seaweed-derived compounds as a valuable resource for combating neurodegenerative diseases across scientific domains. ,Leonel Pereira, Ana Valado [PublishedText] => Published [IsEdit] => 0 [AccountId] => 78 [Zh] => 1 [AuthorsName] => Leonel Pereira, Ana Valado ) [58] => Array ( [ArticleId] => 958 [Create_Time] => 2023-11-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202311/20231129062959.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100459/100459.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100459/100459.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100459/100459-cover.png [JournalsId] => 7 [Title] => Further arguments in favor of the biological relevance of purinergic receptors: the novel emergence of a purinergic signature [Abstract] => [AbstractComplete] => [Names] => Cinzia Volonté, Rafael Franco [CName] => [Doi] => 10.37349/ent.2023.00059 [Published] => November 29, 2023 [Viewed] => 505 [Downloaded] => 15 [Subject] => Commentary [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00059 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:429–434 [Recommend] => 0 [Keywords] => Purinergic receptors, purinergic signature, chunking theory, engram, information unit, heteromer [DetailTitle] => [DetailUrl] => [Id] => 100459 [ris] => https://www.explorationpub.com/uploads/Article/A100459/2c53a449e7b388c4c1abe4b0467c325e.ris [bib] => https://www.explorationpub.com/uploads/Article/A100459/17e1e4e9ff7fd85e190e61e74810a62c.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Volonté C, Franco R. Further arguments in favor of the biological relevance of purinergic receptors: the novel emergence of a purinergic signature. Explor Neuroprot Ther. 2023;3:429–34. https://doi.org/10.37349/ent.2023.00059 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-11-28 08:47:31 [Bib_Time] => 2023-11-28 08:47:31 [KeysWordContens] => Further arguments in favor of the biological relevance of purinergic receptors: the novel emergence of a purinergic signature, Purinergic receptors, purinergic signature, chunking theory, engram, information unit, heteromer,,Cinzia Volonté, Rafael Franco [PublishedText] => Published [IsEdit] => 0 [AccountId] => 78 [Zh] => 1 [AuthorsName] => Cinzia Volonté, Rafael Franco ) [59] => Array ( [ArticleId] => 999 [Create_Time] => 2023-12-12 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231228065010.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100460/100460.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100460/100460.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100460/100460-cover.png [JournalsId] => 7 [Title] => Unique cerebrospinal fluid peptides: potential amyotrophic lateral sclerosis biomarkers and etiological factors [Abstract] => Aim: Amyotrophic lateral sclerosis (ALS) is a progressive disease of unknown etiology, characterized by degeneration of motoneurons and skeletal muscle strength decline that progressively evolves [AbstractComplete] =>

Aim:

Amyotrophic lateral sclerosis (ALS) is a progressive disease of unknown etiology, characterized by degeneration of motoneurons and skeletal muscle strength decline that progressively evolves to respiratory failure and death. A key point in the therapeutic approach is to understand the pathological processes associated with disease evolution. In spite of intensive research on the molecular/cellular mechanisms involved in ALS initiation and progression disease etiology, unfortunately, poorly understood and there is no efficient specific/decisive treatment for ALS patients. The aims of the present study are to identify specific factors in the cerebrospinal fluid (CSF) of ALS patients and to test their potential relevance to the etiology of this disease.

Methods:

Peptides were identified by liquid chromatography tandem mass spectrometry (LC-MS/MS). Motor activity of mice was tested by the Rota-rod test and peptide-induced inflammation was assessed by induction nitric oxide synthase activity in BV2 microglia cells.

Results:

Analysis of CSF samples of ALS patients (n = 15) detected two peptides, C-terminal fragments of transthyretin and osteopontin, which were absent in a control group (n = 15). In addition to being potential biomarker candidates, the relevancy of these peptides to the disease etiology was tested by assessing their effects on motor activity in mice and inflammation model in cell culture. Intranasal administration of the peptides reduced motor activity in the Rota-rod test and activated lipopolysaccharide-induced inflammation in BV2 microglia cells.

Conclusions:

These findings suggest that during ALS onset and progression two potentially neurotoxic peptides are formed, released, or penetrated the central nervous system thus inducing neuroinflammation and neurodegeneration.

[Names] => Uri Wormser ... Yoram Finkelstein [CName] => [Doi] => 10.37349/ent.2023.00060 [Published] => December 12, 2023 [Viewed] => 612 [Downloaded] => 24 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00060 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 89 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:435–445 [Recommend] => 0 [Keywords] => Amyotrophic lateral sclerosis, peptides, neuroinflammation, motoneurons, transthyretin, osteopontin [DetailTitle] => Biomarkers in Amyotrophic Lateral Sclerosis [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/89 [Id] => 100460 [ris] => https://www.explorationpub.com/uploads/Article/A100460/af424b49c88a35707e6cf5fe99b847bf.ris [bib] => https://www.explorationpub.com/uploads/Article/A100460/155c09e7428d9245554d6e01c316f20b.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Wormser U, Sintov A, Vinceti M, Mandrioli J, Brodsky B, Proscura E, et al. Unique cerebrospinal fluid peptides: potential amyotrophic lateral sclerosis biomarkers and etiological factors. Explor Neuroprot Ther. 2023;3:435–45. https://doi.org/10.37349/ent.2023.00060 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-12-12 07:08:13 [Bib_Time] => 2023-12-12 07:08:13 [KeysWordContens] => Unique cerebrospinal fluid peptides: potential amyotrophic lateral sclerosis biomarkers and etiological factors, Amyotrophic lateral sclerosis, peptides, neuroinflammation, motoneurons, transthyretin, osteopontin, Aim: Amyotrophic lateral sclerosis (ALS) is a progressive disease of unknown etiology, characterized by degeneration of motoneurons and skeletal muscle strength decline that progressively evolves to respiratory failure and death. A key point in the therapeutic approach is to understand the pathological processes associated with disease evolution. In spite of intensive research on the molecular/cellular mechanisms involved in ALS initiation and progression disease etiology, unfortunately, poorly understood and there is no efficient specific/decisive treatment for ALS patients. The aims of the present study are to identify specific factors in the cerebrospinal fluid (CSF) of ALS patients and to test their potential relevance to the etiology of this disease. Methods: Peptides were identified by liquid chromatography tandem mass spectrometry (LC-MS/MS). Motor activity of mice was tested by the Rota-rod test and peptide-induced inflammation was assessed by induction nitric oxide synthase activity in BV2 microglia cells. Results: Analysis of CSF samples of ALS patients (n = 15) detected two peptides, C-terminal fragments of transthyretin and osteopontin, which were absent in a control group (n = 15). In addition to being potential biomarker candidates, the relevancy of these peptides to the disease etiology was tested by assessing their effects on motor activity in mice and inflammation model in cell culture. Intranasal administration of the peptides reduced motor activity in the Rota-rod test and activated lipopolysaccharide-induced inflammation in BV2 microglia cells. Conclusions: These findings suggest that during ALS onset and progression two potentially neurotoxic peptides are formed, released, or penetrated the central nervous system thus inducing neuroinflammation and neurodegeneration. ,Uri Wormser ... Yoram Finkelstein [PublishedText] => Published [IsEdit] => 0 [AccountId] => 78 [Zh] => 1 [AuthorsName] => Uri Wormser, Amnon Sintov, Marco Vinceti, Jessica Mandrioli, Berta Brodsky, Elena Proscura, Yoram Finkelstein ) [60] => Array ( [ArticleId] => 1003 [Create_Time] => 2023-12-13 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231213083054.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100461/100461.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100461/100461.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100461/cover.png [JournalsId] => 7 [Title] => Minimum spanning tree analysis for epilepsy magnetoencephalography (MEG) data [Abstract] => Aim: Recently, brain network research is actively conducted through the application of graph theory. However, comparison between brain networks is subject to bias issues due to topological charac [AbstractComplete] =>

Aim:

Recently, brain network research is actively conducted through the application of graph theory. However, comparison between brain networks is subject to bias issues due to topological characteristics and heterogeneity across subjects. The minimum spanning tree (MST) is a method that is increasingly applied to overcome the thresholding problem. In this study, the aim is to use the MST analysis in comparing epilepsy patients and controls to find the differences between groups.

Methods:

The MST combines entities for epileptic magnetoencephalography (MEG) data. The MST was applied and compared to 21 left surgery (LT) and 21 right surgery (RT) patients with epilepsy and good postoperative prognosis and a healthy control (HC) group. MST metrics such as betweenness centrality, eccentricity, diameter, and leaf fraction, are computed and compared to describe the integration and efficiency of the network. The MST analysis is applied to each subject, and then the integrated MST is obtained using the distance concept. This approach can be advantageous when comparing the topological structure of patients to controls with the same number of nodes.

Results:

The HC group showed less topological change and more network efficiency than the epilepsy LT and RT groups. In addition, the posterior cingulate gyrus was found as a hub node only in the patient group in individual and integrated subject data analysis.

Conclusions:

This study suggests propose that the hippocampus borrows from the default network when one side fails, compensating for the weakened function.

[Names] => Sunhan Shin ... Jaehee Kim [CName] => [Doi] => 10.37349/ent.2023.00061 [Published] => December 13, 2023 [Viewed] => 662 [Downloaded] => 16 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00061 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 142 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:446–456 [Recommend] => 0 [Keywords] => Brain network, epilepsy, magnetoencephalography (MEG), MEG network, minimum spanning tree [DetailTitle] => New Advances in Imaging Techniques for the Evaluation of Neurological Disorders [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/142 [Id] => 100461 [ris] => https://www.explorationpub.com/uploads/Article/A100461/a55b9297b1a93a666380c0ccc95c80bc.ris [bib] => https://www.explorationpub.com/uploads/Article/A100461/ca006345d4a982a78954eef47a2012c0.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Shin S, Chung CK, Kim J. Minimum spanning tree analysis for epilepsy magnetoencephalography (MEG) data. Explor Neuroprot Ther. 2023;3:446–56. https://doi.org/10.37349/ent.2023.00061 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-12-13 08:30:55 [Bib_Time] => 2023-12-13 08:30:55 [KeysWordContens] => Minimum spanning tree analysis for epilepsy magnetoencephalography (MEG) data, Brain network, epilepsy, magnetoencephalography (MEG), MEG network, minimum spanning tree, Aim: Recently, brain network research is actively conducted through the application of graph theory. However, comparison between brain networks is subject to bias issues due to topological characteristics and heterogeneity across subjects. The minimum spanning tree (MST) is a method that is increasingly applied to overcome the thresholding problem. In this study, the aim is to use the MST analysis in comparing epilepsy patients and controls to find the differences between groups. Methods: The MST combines entities for epileptic magnetoencephalography (MEG) data. The MST was applied and compared to 21 left surgery (LT) and 21 right surgery (RT) patients with epilepsy and good postoperative prognosis and a healthy control (HC) group. MST metrics such as betweenness centrality, eccentricity, diameter, and leaf fraction, are computed and compared to describe the integration and efficiency of the network. The MST analysis is applied to each subject, and then the integrated MST is obtained using the distance concept. This approach can be advantageous when comparing the topological structure of patients to controls with the same number of nodes. Results: The HC group showed less topological change and more network efficiency than the epilepsy LT and RT groups. In addition, the posterior cingulate gyrus was found as a hub node only in the patient group in individual and integrated subject data analysis. Conclusions: This study suggests propose that the hippocampus borrows from the default network when one side fails, compensating for the weakened function. ,Sunhan Shin ... Jaehee Kim [PublishedText] => Published [IsEdit] => 0 [AccountId] => 79 [Zh] => 1 [AuthorsName] => Sunhan Shin, Chun Kee Chung, Jaehee Kim ) [61] => Array ( [ArticleId] => 1021 [Create_Time] => 2023-12-22 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231225035407.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100462/100462.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100462/100462.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100462/100462_cover.png [JournalsId] => 7 [Title] => Hyperbaric oxygen therapy—a new hope for Alzheimer’s patients: a case report and literature review [Abstract] => The currently available pharmacological anti-dementia treatments provide only temporary and limited benefits. Not surprisingly, patients and professionals increasingly explore non-pharmacological in [AbstractComplete] =>

The currently available pharmacological anti-dementia treatments provide only temporary and limited benefits. Not surprisingly, patients and professionals increasingly explore non-pharmacological interventions that may alleviate dementia symptoms. Among these interventions is hyperbaric oxygen therapy (HBOT). A brief review is presented on HBOT use in medicine, with its mode of action in dementia, specifically Alzheimer’s disease, as well as a case report of self-initiated HBOT in a 62-year-old man with a clinical diagnosis of probable Alzheimer’s disease. He had over 400 HBOT sessions [2–3 times weekly, with a duration of 30–50 min, in a multi-place hyperbaric chamber at 2 atmospheres absolute (ATA)] over 7 years and use of donepezil (10 mg daily) for the last 3 years when formally diagnosed by the National Health Service (NHS) Memory Service. The patient’s longitudinal neurocognitive and neuroradiological evidence over 7 years of follow-up remained stable (with no major cognitive decline and no behavioral changes) when compared to his initial presentation when diagnosed by the private health provider. His driving remains unimpaired, and he continues to be independent. This highlights the potential HBOT benefits including those on visuospatial ability and activities of daily living in people with Alzheimer’s disease. This case report argues for more extensive research into the clinical effects of HBOT in Alzheimer’s disease. Discussion of HBOT use is along with the latest advances in anti-amyloid immunotherapy for Alzheimer’s disease, as well as HBOT augmentation of current and novel dementia drug delivery via nanotechnology.

[Names] => Elizabeta B. Mukaetova-Ladinska ... Qadeer Arshad [CName] => [Doi] => 10.37349/ent.2023.00062 [Published] => December 22, 2023 [Viewed] => 1129 [Downloaded] => 22 [Subject] => Case Report [Year] => 2023 [CiteUrl] => https://doi.org/10.37349/ent.2023.00062 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 228 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:457–469 [Recommend] => 0 [Keywords] => Hyperbaric oxygen therapy, Alzheimer’s disease, dementia, non-pharmacological treatment, nanomedicine [DetailTitle] => Defending the Brain and the Mind: Exploring Neuroprotective Therapies for Mental Health Disorders [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/228 [Id] => 100462 [ris] => https://www.explorationpub.com/uploads/Article/A100462/f88b1707f2f9d7becb1e02b06379e460.ris [bib] => https://www.explorationpub.com/uploads/Article/A100462/c1a0c2cdc3df9ea43e4ecae82c8c1786.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Mukaetova-Ladinska EB, Steptoe J, Critchfield M, Yoon HJ, Sharif M, Arshad Q. Hyperbaric oxygen therapy—a new hope for Alzheimer’s patients: a case report and literature review. Explor Neuroprot Ther. 2023;3:457–69. https://doi.org/10.37349/ent.2023.00062 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-12-25 03:54:07 [Bib_Time] => 2023-12-25 03:54:07 [KeysWordContens] => Hyperbaric oxygen therapy—a new hope for Alzheimer’s patients: a case report and literature review, Hyperbaric oxygen therapy, Alzheimer’s disease, dementia, non-pharmacological treatment, nanomedicine, The currently available pharmacological anti-dementia treatments provide only temporary and limited benefits. Not surprisingly, patients and professionals increasingly explore non-pharmacological interventions that may alleviate dementia symptoms. Among these interventions is hyperbaric oxygen therapy (HBOT). A brief review is presented on HBOT use in medicine, with its mode of action in dementia, specifically Alzheimer’s disease, as well as a case report of self-initiated HBOT in a 62-year-old man with a clinical diagnosis of probable Alzheimer’s disease. He had over 400 HBOT sessions [2–3 times weekly, with a duration of 30–50 min, in a multi-place hyperbaric chamber at 2 atmospheres absolute (ATA)] over 7 years and use of donepezil (10 mg daily) for the last 3 years when formally diagnosed by the National Health Service (NHS) Memory Service. The patient’s longitudinal neurocognitive and neuroradiological evidence over 7 years of follow-up remained stable (with no major cognitive decline and no behavioral changes) when compared to his initial presentation when diagnosed by the private health provider. His driving remains unimpaired, and he continues to be independent. This highlights the potential HBOT benefits including those on visuospatial ability and activities of daily living in people with Alzheimer’s disease. This case report argues for more extensive research into the clinical effects of HBOT in Alzheimer’s disease. Discussion of HBOT use is along with the latest advances in anti-amyloid immunotherapy for Alzheimer’s disease, as well as HBOT augmentation of current and novel dementia drug delivery via nanotechnology. ,Elizabeta B. Mukaetova-Ladinska ... Qadeer Arshad [PublishedText] => Published [IsEdit] => 0 [AccountId] => 85 [Zh] => 1 [AuthorsName] => Elizabeta B. Mukaetova-Ladinska, Joanna Steptoe, Matthew Critchfield, Ha-Jun Yoon, Mishaal Sharif, Qadeer Arshad ) [62] => Array ( [ArticleId] => 1029 [Create_Time] => 2023-12-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231226084533.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100463/100463.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100463/100463.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100463/ent-03-100463_cover.png [JournalsId] => 7 [Title] => Effectiveness of dry needling on the treatment of patients with multiple sclerosis: systematic review [Abstract] => Aim: The aim of this study is to review the effectiveness of dry needling in patients with multiple sclerosis (MS). Methods: PubMed, Physiotherapy Evidence Database (PEDro), Web of Science, [AbstractComplete] =>

Aim:

The aim of this study is to review the effectiveness of dry needling in patients with multiple sclerosis (MS).

Methods:

PubMed, Physiotherapy Evidence Database (PEDro), Web of Science, Scopus, and Cochrane Library databases were searched from its inception until July 2023 and the reference lists of the articles obtained were manually searched. Studies examining the effectiveness of dry needling treatment alone or in combination with a different protocol in individuals diagnosed with MS, regardless of type, were included. The systematic review included quasi-experimental studies and case reports. Studies involving traditional Chinese medicine acupuncture applications, conference abstracts, and protocol records were excluded. Methodological quality assessments were carried out independently by two authors using tools developed by the Joanna Briggs Institute (JBI).

Results:

A total of 130 studies were found in the searches. Some studies were excluded due to duplication, protocol registration, conference abstract, and content outside the scope of the study and 7 studies were included in the review. In total, 33 individuals were included in this review, 22 of whom were women. Four studies specified the MS type of the patients, while the other studies did not specify MS type.

Conclusions:

Despite some limitations, this is, to our knowledge, the first review summarizing studies evaluating the effectiveness of dry needling in MS patients. The dry needling technique alone or in a combination of treatments was effective in improving pain, spasticity, range of motion, dexterity, mobility, limb function, and quality of life in MS patients. However, these results should be treated with caution due to the small number of included studies and the lack of randomized controlled trials. Although it is too early to talk about the positive effects of the dry needling technique in MS patients, the study results are promising. More randomized controlled trials should be conducted on this topic.

[Names] => Ali Mutlu ... Buket Büyükturan [CName] => [Doi] => 10.37349/ent.2023.00063 [Published] => December 26, 2023 [Viewed] => 650 [Downloaded] => 26 [Subject] => Systematic Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00063 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 57 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:470–480 [Recommend] => 0 [Keywords] => Dry needling, mobility, multiple sclerosis, pain, spasticity, quality of life [DetailTitle] => Dry Needling for Neurological Disorders [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/57 [Id] => 100463 [ris] => https://www.explorationpub.com/uploads/Article/A100463/f0726c1929f82b94a95d1de52a2799fb.ris [bib] => https://www.explorationpub.com/uploads/Article/A100463/75353874dc9047bc2f8149fbb975c539.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Mutlu A, Kaya MH, Büyükturan Ö, Büyükturan B. Effectiveness of dry needling on the treatment of patients with multiple sclerosis: systematic review. Explor Neuroprot Ther. 2023;3:470–80. https://doi.org/10.37349/ent.2023.00063 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-12-26 06:14:47 [Bib_Time] => 2023-12-26 06:14:47 [KeysWordContens] => Effectiveness of dry needling on the treatment of patients with multiple sclerosis: systematic review, Dry needling, mobility, multiple sclerosis, pain, spasticity, quality of life, Aim: The aim of this study is to review the effectiveness of dry needling in patients with multiple sclerosis (MS). Methods: PubMed, Physiotherapy Evidence Database (PEDro), Web of Science, Scopus, and Cochrane Library databases were searched from its inception until July 2023 and the reference lists of the articles obtained were manually searched. Studies examining the effectiveness of dry needling treatment alone or in combination with a different protocol in individuals diagnosed with MS, regardless of type, were included. The systematic review included quasi-experimental studies and case reports. Studies involving traditional Chinese medicine acupuncture applications, conference abstracts, and protocol records were excluded. Methodological quality assessments were carried out independently by two authors using tools developed by the Joanna Briggs Institute (JBI). Results: A total of 130 studies were found in the searches. Some studies were excluded due to duplication, protocol registration, conference abstract, and content outside the scope of the study and 7 studies were included in the review. In total, 33 individuals were included in this review, 22 of whom were women. Four studies specified the MS type of the patients, while the other studies did not specify MS type. Conclusions: Despite some limitations, this is, to our knowledge, the first review summarizing studies evaluating the effectiveness of dry needling in MS patients. The dry needling technique alone or in a combination of treatments was effective in improving pain, spasticity, range of motion, dexterity, mobility, limb function, and quality of life in MS patients. However, these results should be treated with caution due to the small number of included studies and the lack of randomized controlled trials. Although it is too early to talk about the positive effects of the dry needling technique in MS patients, the study results are promising. More randomized controlled trials should be conducted on this topic. ,Ali Mutlu ... Buket Büyükturan [PublishedText] => Published [IsEdit] => 0 [AccountId] => 24 [Zh] => 1 [AuthorsName] => Ali Mutlu, Mehmet Hanifi Kaya, Öznur Büyükturan, Buket Büyükturan ) [63] => Array ( [ArticleId] => 1030 [Create_Time] => 2023-12-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231226090640.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100464/100464.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100464/100464.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100464/100464_cover.png [JournalsId] => 7 [Title] => Effects of acoustic neurostimulation in healthy adults on symptoms of depression, anxiety, stress and sleep quality: a randomized clinical study [Abstract] => Aim: To evaluate the application of an acoustic neurostimulation program with binaural beats and isochronic tones isolated or in association, and its effects on sleep, depression, anxiety, and st [AbstractComplete] =>

Aim:

To evaluate the application of an acoustic neurostimulation program with binaural beats and isochronic tones isolated or in association, and its effects on sleep, depression, anxiety, and stress in healthy workers.

Methods:

A randomized, single-blind, parallel-group clinical trial, using acoustic neurostimulation with binaural beats, isochronic tones, or a combination of these in the 10 Hz range (alpha) performed with daily 20-minute sessions for 21 days. Changes in brainwave patterns were assessed by electroencephalogram (EEG). Psycho-emotional state was assessed with the Depression, Anxiety and Stress Scale 21 Items (DASS-21), and sleep quality with the Pittsburgh Sleep Quality Index (PSQI). In addition, salivary cortisol levels were evaluated as a biomarker of stress.

Results:

The data revealed distinct patterns of brainwave modulation via brainwave entrainment (BWE) techniques. Binaural beats and isochronic tones, alone and in combination, effectively increased alpha brainwaves in the temporoparietal region. However, when assessing theta brainwave frequencies in the same region, only binaural beats showed a significant effect. Furthermore, in the prefrontal cortex, an elevation in beta waves was exclusively observed with the use of binaural beats. These findings underscore the specificity of BWE techniques on different brainwave frequencies and regions. The study demonstrated marked improvements in several symptoms related to stress, depression, anxiety, assessed by psychometry with DASS-21 and related to sleep quality assessed by the PSQI.

Conclusions:

These results indicate that 10 Hz acoustic neurostimulation in the alpha range, whether through binaural beats, isochronic tones, or a combination of both, can significantly influence brainwave patterns and intensity. Notably, participants exhibited decrease in symptoms of stress, depression, and anxiety, coupled with improved sleep quality. These data suggest that alpha acoustic neurostimulation holds promise as an effective intervention for bolstering mood, mental health, and overall emotional well-being [Brazilian Clinical Trials Registry (ReBec, ensaiosclinicos.gov.br) identifier: RBR-10yj42dj].

[Names] => Sandro A. Kanzler ... Rui Daniel Prediger [CName] => [Doi] => 10.37349/ent.2023.00064 [Published] => December 26, 2023 [Viewed] => 830 [Downloaded] => 43 [Subject] => Original Article [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/ent.2023.00064 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:481–496 [Recommend] => 0 [Keywords] => Acoustic neurostimulation, sleep, stress, anxiety, depression [DetailTitle] => [DetailUrl] => [Id] => 100464 [ris] => https://www.explorationpub.com/uploads/Article/A100464/24386c4ead163b5281b412f4443b48ee.ris [bib] => https://www.explorationpub.com/uploads/Article/A100464/6a8cf06b5d7a154e689c726a8f386d03.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Kanzler SA, Cidral-Filho FJ, Kuerten B, Prediger RD. Effects of acoustic neurostimulation in healthy adults on symptoms of depression, anxiety, stress and sleep quality: a randomized clinical study. Explor Neuroprot Ther. 2023;3:481–96. https://doi.org/10.37349/ent.2023.00064 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-12-25 05:31:05 [Bib_Time] => 2023-12-25 05:31:05 [KeysWordContens] => Effects of acoustic neurostimulation in healthy adults on symptoms of depression, anxiety, stress and sleep quality: a randomized clinical study, Acoustic neurostimulation, sleep, stress, anxiety, depression, Aim: To evaluate the application of an acoustic neurostimulation program with binaural beats and isochronic tones isolated or in association, and its effects on sleep, depression, anxiety, and stress in healthy workers. Methods: A randomized, single-blind, parallel-group clinical trial, using acoustic neurostimulation with binaural beats, isochronic tones, or a combination of these in the 10 Hz range (alpha) performed with daily 20-minute sessions for 21 days. Changes in brainwave patterns were assessed by electroencephalogram (EEG). Psycho-emotional state was assessed with the Depression, Anxiety and Stress Scale 21 Items (DASS-21), and sleep quality with the Pittsburgh Sleep Quality Index (PSQI). In addition, salivary cortisol levels were evaluated as a biomarker of stress. Results: The data revealed distinct patterns of brainwave modulation via brainwave entrainment (BWE) techniques. Binaural beats and isochronic tones, alone and in combination, effectively increased alpha brainwaves in the temporoparietal region. However, when assessing theta brainwave frequencies in the same region, only binaural beats showed a significant effect. Furthermore, in the prefrontal cortex, an elevation in beta waves was exclusively observed with the use of binaural beats. These findings underscore the specificity of BWE techniques on different brainwave frequencies and regions. The study demonstrated marked improvements in several symptoms related to stress, depression, anxiety, assessed by psychometry with DASS-21 and related to sleep quality assessed by the PSQI. Conclusions: These results indicate that 10 Hz acoustic neurostimulation in the alpha range, whether through binaural beats, isochronic tones, or a combination of both, can significantly influence brainwave patterns and intensity. Notably, participants exhibited decrease in symptoms of stress, depression, and anxiety, coupled with improved sleep quality. These data suggest that alpha acoustic neurostimulation holds promise as an effective intervention for bolstering mood, mental health, and overall emotional well-being [Brazilian Clinical Trials Registry (ReBec, ensaiosclinicos.gov.br) identifier: RBR-10yj42dj]. ,Sandro A. Kanzler ... Rui Daniel Prediger [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 1 [AuthorsName] => Sandro A. Kanzler, Francisco J. Cidral-Filho, Beatriz Kuerten, Rui Daniel Prediger ) [64] => Array ( [ArticleId] => 1038 [Create_Time] => 2023-12-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231227021237.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100465/100465.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100465/100465.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100465/cover.png [JournalsId] => 7 [Title] => Breaking the amyotrophic lateral sclerosis early diagnostic barrier: the promise of general markers [Abstract] => Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disease that is associated with selective and progressive loss of motor neurons. As a consequence, the symptoms of ALS are muscle cr [AbstractComplete] =>

Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disease that is associated with selective and progressive loss of motor neurons. As a consequence, the symptoms of ALS are muscle cramps and weakness, and it eventually leads to death. The general markers for early diagnosis can assist ALS patients in receiving early intervention and prolonging their survival. Recently, some novel approaches or previously suggested methods have validated the potential for early diagnosis of ALS. The purpose of this review is to summarize the status of current general markers discovery and development for early diagnosis of ALS, including genes, proteins neuroimaging, neurophysiology, neuroultrasound, and machine learning models. The main genetic markers evaluated are superoxide dismutase 1 (SOD1), chromosome 9 open reading frame 72 (C9orf72), transactivation-responsive DNA binding protein 43 (TARDBP), and fused in sarcoma (FUS) genes. Among proteins, neurofilament light chain is still the most established disease-specific adaptive change in ALS. The expression of chitinases, glial fibrillary acidic protein (GFAP), and inflammatory factors are changed in the early stage of ALS. Besides, more patient-friendly and accessible feature assays are explored by the development of neuroimaging, neurophysiology, and neuroultrasound techniques. The novel disease-specific changes exhibited the promising potential for early diagnosis of ALS. All of these general markers still have limitations in the early diagnosis, therefore there is an urgent need for the validation and development of new disease-specific features for ALS.

[Names] => Yizhou Lu ... Qinming Zhou [CName] => [Doi] => 10.37349/ent.2023.00065 [Published] => December 27, 2023 [Viewed] => 650 [Downloaded] => 33 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00065 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 89 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:497–512 [Recommend] => 0 [Keywords] => Amyotrophic lateral sclerosis, marker, genes, neurofilament, magnetic resonance imaging, positron emission tomography, neurophysiology, neuroultrasound [DetailTitle] => Biomarkers in Amyotrophic Lateral Sclerosis [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/89 [Id] => 100465 [ris] => https://www.explorationpub.com/uploads/Article/A100465/785d61074775186b2dd5522cdd0264ae.ris [bib] => https://www.explorationpub.com/uploads/Article/A100465/d7fbfd3705ef824268f3a0073c9619ca.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Lu Y, He L, Meng H, Chen S, Zhou Q. Breaking the amyotrophic lateral sclerosis early diagnostic barrier: the promise of general markers. Explor Neuroprot Ther. 2023;3:497–512. https://doi.org/10.37349/ent.2023.00065 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-12-27 02:12:37 [Bib_Time] => 2023-12-27 02:12:37 [KeysWordContens] => Breaking the amyotrophic lateral sclerosis early diagnostic barrier: the promise of general markers, Amyotrophic lateral sclerosis, marker, genes, neurofilament, magnetic resonance imaging, positron emission tomography, neurophysiology, neuroultrasound, Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disease that is associated with selective and progressive loss of motor neurons. As a consequence, the symptoms of ALS are muscle cramps and weakness, and it eventually leads to death. The general markers for early diagnosis can assist ALS patients in receiving early intervention and prolonging their survival. Recently, some novel approaches or previously suggested methods have validated the potential for early diagnosis of ALS. The purpose of this review is to summarize the status of current general markers discovery and development for early diagnosis of ALS, including genes, proteins neuroimaging, neurophysiology, neuroultrasound, and machine learning models. The main genetic markers evaluated are superoxide dismutase 1 (SOD1), chromosome 9 open reading frame 72 (C9orf72), transactivation-responsive DNA binding protein 43 (TARDBP), and fused in sarcoma (FUS) genes. Among proteins, neurofilament light chain is still the most established disease-specific adaptive change in ALS. The expression of chitinases, glial fibrillary acidic protein (GFAP), and inflammatory factors are changed in the early stage of ALS. Besides, more patient-friendly and accessible feature assays are explored by the development of neuroimaging, neurophysiology, and neuroultrasound techniques. The novel disease-specific changes exhibited the promising potential for early diagnosis of ALS. All of these general markers still have limitations in the early diagnosis, therefore there is an urgent need for the validation and development of new disease-specific features for ALS. ,Yizhou Lu ... Qinming Zhou [PublishedText] => Published [IsEdit] => 0 [AccountId] => 79 [Zh] => 1 [AuthorsName] => Yizhou Lu, Lu He, Huanyu Meng, Sheng Chen, Qinming Zhou ) [65] => Array ( [ArticleId] => 1048 [Create_Time] => 2023-12-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231229084335.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100466/100466.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100466/100466.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100466/100466_cover.png [JournalsId] => 7 [Title] => Retraction: Diffusion magnetic resonance imaging-based surrogate marker in amyotrophic lateral sclerosis [Abstract] => [AbstractComplete] => [Names] => Editorial Office [CName] => [Doi] => 10.37349/ent.2023.00066 [Published] => December 29, 2023 [Viewed] => 445 [Downloaded] => 27 [Subject] => Retraction [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2023.00066 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2023;3:513 [Recommend] => 0 [Keywords] => [DetailTitle] => [DetailUrl] => [Id] => 100466 [ris] => https://www.explorationpub.com/uploads/Article/A100466/df48c2929fbc5050a369d7df87e45751.ris [bib] => https://www.explorationpub.com/uploads/Article/A100466/bc19719f2b169f7bc684862c476070a3.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Editorial Office. Retraction: Diffusion magnetic resonance imaging-based surrogate marker in amyotrophic lateral sclerosis. Explor Neuroprot Ther. 2023;3:513. https://doi.org/10.37349/ent.2023.00066 [Jindex] => 0 [CEmail] => [Ris_Time] => 2023-12-26 08:10:16 [Bib_Time] => 2023-12-26 08:10:16 [KeysWordContens] => Retraction: Diffusion magnetic resonance imaging-based surrogate marker in amyotrophic lateral sclerosis,,,Editorial Office [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 [AuthorsName] => ) [66] => Array ( [ArticleId] => 1120 [Create_Time] => 2024-02-21 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240221094318.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100467/100467.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100467/100467.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100467/ent-04-100467_cover.png [JournalsId] => 7 [Title] => Therapeutic exercise in fibromyalgia syndrome: a narrative review [Abstract] => Fibromyalgia syndrome (FMS) is characterised by the presence of distributed pain in different areas of the body accompanied by the alteration of some functions such as the activity of the neuroveget [AbstractComplete] =>

Fibromyalgia syndrome (FMS) is characterised by the presence of distributed pain in different areas of the body accompanied by the alteration of some functions such as the activity of the neurovegetative system, the sleep quality, or the presence of fatigue. The present narrative review aims to evaluate some key studies regarding the effects of different therapeutic exercise (TE) modalities on clinical variables of interest in patients with FMS, as well as to discuss some of the possible mechanisms of action of TE in improving pain intensity in patients with FMS. All aerobic, strengthening, and body-mind exercises were shown to bring about changes in the improvement of clinical variables of interest in patients with FMS. In addition, with regard to the improvement of pain intensity, there are different arguments that could explain the hypoalgesic effect of TE (structured in physical, neurophysiological, and psychosocial mechanisms). In conclusion, TE is a clinical tool with great potential for patients with FMS as it may produce hypoalgesia through physical, neurophysiological, and psychosocial mechanisms. All these TE modalities have demonstrated in isolation a remarkable effectiveness in the overall improvement of patients with FMS. However, more research is needed in this field especially on the long-term effects and on the combination of the different training modalities.

[Names] => Carlos Forner-Álvarez ... Núria Sempere-Rubio [CName] => [Doi] => 10.37349/ent.2024.00067 [Published] => February 20, 2024 [Viewed] => 599 [Downloaded] => 25 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00067 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 147 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:1–10 [Recommend] => 0 [Keywords] => Therapeutic exercise, fibromyalgia syndrome, narrative review [DetailTitle] => Empower Yourself - Physical Activity as Prevention and Rehabilitation of Neurological and Psychiatric Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/147 [Id] => 100467 [ris] => https://www.explorationpub.com/uploads/Article/A100467/d3ac6a219b9ff7e33b05088208021656.ris [bib] => https://www.explorationpub.com/uploads/Article/A100467/87093275dbcc551095dfeef034a61742.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Forner-Álvarez C, Zanón-Chanzá C, Cuenca-Martínez F, Sempere-Rubio N. Therapeutic exercise in fibromyalgia syndrome: a narrative review. Explor Neuroprot Ther. 2024;4:1–10. https://doi.org/10.37349/ent.2024.00067 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-02-21 09:33:18 [Bib_Time] => 2024-02-21 09:33:18 [KeysWordContens] => Therapeutic exercise in fibromyalgia syndrome: a narrative review, Therapeutic exercise, fibromyalgia syndrome, narrative review, Fibromyalgia syndrome (FMS) is characterised by the presence of distributed pain in different areas of the body accompanied by the alteration of some functions such as the activity of the neurovegetative system, the sleep quality, or the presence of fatigue. The present narrative review aims to evaluate some key studies regarding the effects of different therapeutic exercise (TE) modalities on clinical variables of interest in patients with FMS, as well as to discuss some of the possible mechanisms of action of TE in improving pain intensity in patients with FMS. All aerobic, strengthening, and body-mind exercises were shown to bring about changes in the improvement of clinical variables of interest in patients with FMS. In addition, with regard to the improvement of pain intensity, there are different arguments that could explain the hypoalgesic effect of TE (structured in physical, neurophysiological, and psychosocial mechanisms). In conclusion, TE is a clinical tool with great potential for patients with FMS as it may produce hypoalgesia through physical, neurophysiological, and psychosocial mechanisms. All these TE modalities have demonstrated in isolation a remarkable effectiveness in the overall improvement of patients with FMS. However, more research is needed in this field especially on the long-term effects and on the combination of the different training modalities. ,Carlos Forner-Álvarez ... Núria Sempere-Rubio [PublishedText] => Published [IsEdit] => 0 [AccountId] => 24 [Zh] => 1 [AuthorsName] => Carlos Forner-Álvarez, Carlos Zanón-Chanzá, Ferran Cuenca-Martínez, Núria Sempere-Rubio ) [67] => Array ( [ArticleId] => 1133 [Create_Time] => 2024-02-23 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240223083432.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100468/100468.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100468/100468.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100468/100468_cover.png [JournalsId] => 7 [Title] => Resolving a paradox: antidepressants, neuroinflammation, and neurodegeneration [Abstract] => Depression is a known risk factor for dementia. Antidepressants are the most commonly used treatment for this condition, and are effective in at least half to two-thirds of cases. Extensive evidence [AbstractComplete] =>

Depression is a known risk factor for dementia. Antidepressants are the most commonly used treatment for this condition, and are effective in at least half to two-thirds of cases. Extensive evidence from in vitro and animal models suggests that antidepressants have anti-inflammatory and neuroprotective properties. These effects have been shown to reduce the oxidative damage, amyloid aggregation, and expression of pro-inflammatory genes associated with animal models of neurodegenerative disorders. However, longitudinal research in humans has shown that antidepressants do not protect against dementia, and may even be associated with a risk of cognitive deterioration over time in older adults. The contrast between two sets of findings represents a paradox of significant clinical and public health significance, particularly when treating depression in late life. This review paper attempts to resolve this paradox by critically reviewing the medium- and long-term effects of antidepressants on peripheral immune-inflammatory responses, infection risk, gut microbiota, and neuroendocrine responses to stress, and how these effects may influence the risk of neurodegeneration. Briefly stated, it is possible that the peripheral actions of antidepressant medications may antagonize their beneficial effects against neuroinflammation. The implications of these findings are then explored with a particular focus on the development and testing of multimodal neuroprotective and anti-inflammatory treatments that could reduce the risk of Alzheimer’s and related dementias in patients suffering from depression.

[Names] => Ravi Philip Rajkumar [CName] => [Doi] => 10.37349/ent.2024.00068 [Published] => February 23, 2024 [Viewed] => 731 [Downloaded] => 37 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00068 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 224 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:11–37 [Recommend] => 0 [Keywords] => Antidepressants, neuroinflammation, neurodegeneration, Alzheimer’s disease, cytokines, infection, gut-brain axis, hypothalamic-pituitary-adrenal axis [DetailTitle] => Neuro-Inflammation as a Target in the Design of Multifunctional Drug Candidates for Neurodegenerative Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/224 [Id] => 100468 [ris] => https://www.explorationpub.com/uploads/Article/A100468/0e48de07033be1763ed305ce79e30f4a.ris [bib] => https://www.explorationpub.com/uploads/Article/A100468/ac69b71b8371ac0d306e4209b7553c0a.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Rajkumar RP. Resolving a paradox: antidepressants, neuroinflammation, and neurodegeneration. Explor Neuroprot Ther. 2024;4:11–37. https://doi.org/10.37349/ent.2024.00068 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-02-23 08:34:32 [Bib_Time] => 2024-02-23 08:34:32 [KeysWordContens] => Resolving a paradox: antidepressants, neuroinflammation, and neurodegeneration, Antidepressants, neuroinflammation, neurodegeneration, Alzheimer’s disease, cytokines, infection, gut-brain axis, hypothalamic-pituitary-adrenal axis, Depression is a known risk factor for dementia. Antidepressants are the most commonly used treatment for this condition, and are effective in at least half to two-thirds of cases. Extensive evidence from in vitro and animal models suggests that antidepressants have anti-inflammatory and neuroprotective properties. These effects have been shown to reduce the oxidative damage, amyloid aggregation, and expression of pro-inflammatory genes associated with animal models of neurodegenerative disorders. However, longitudinal research in humans has shown that antidepressants do not protect against dementia, and may even be associated with a risk of cognitive deterioration over time in older adults. The contrast between two sets of findings represents a paradox of significant clinical and public health significance, particularly when treating depression in late life. This review paper attempts to resolve this paradox by critically reviewing the medium- and long-term effects of antidepressants on peripheral immune-inflammatory responses, infection risk, gut microbiota, and neuroendocrine responses to stress, and how these effects may influence the risk of neurodegeneration. Briefly stated, it is possible that the peripheral actions of antidepressant medications may antagonize their beneficial effects against neuroinflammation. The implications of these findings are then explored with a particular focus on the development and testing of multimodal neuroprotective and anti-inflammatory treatments that could reduce the risk of Alzheimer’s and related dementias in patients suffering from depression. ,Ravi Philip Rajkumar [PublishedText] => Published [IsEdit] => 0 [AccountId] => 79 [Zh] => 1 [AuthorsName] => Ravi Philip Rajkumar ) [68] => Array ( [ArticleId] => 1137 [Create_Time] => 2024-02-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240227080916.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100469/100469.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100469/100469.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100469/100469_cover.png [JournalsId] => 7 [Title] => The diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in children [Abstract] => Over the last two decades, immunoglobulin G (IgG) antibodies against myelin oligodendrocyte glycoprotein (MOG), previously thought to be a biomarker of multiple sclerosis (MS), have been shown to ca [AbstractComplete] =>

Over the last two decades, immunoglobulin G (IgG) antibodies against myelin oligodendrocyte glycoprotein (MOG), previously thought to be a biomarker of multiple sclerosis (MS), have been shown to cause a distinct disease called MOG antibody-associated disease (MOGAD). MOGAD accounts for approximately one-third of all demyelinating syndromes in children and is the second most common central nervous system (CNS) demyelinating disease after MS. The diagnosis is made by detecting anti-MOG IgG antibodies against the natural MOG antigen, in the presence of compatible clinical and neuroradiological features. However, due to controversies in the methodologies for detecting anti-MOG antibodies and their diagnostic cutoff values, as well as the expanding clinical spectrum, accurate diagnosis may be challenging, at least in a subset of patients. Clinical presentations of MOGAD vary by age; the highest rates are seen in acute disseminated encephalomyelitis in younger children and optic neuritis, myelitis, or brainstem symptoms in older children. Although it was previously thought to be a milder demyelinating disorder and to have a monophasic course in the majority of patients, recent studies have shown that relapses occur in about half of the patients and sequelae develop in a significant proportion of them, especially in those with persistently high antibody titers, leukodystrophy-like magnetic resonance imaging (MRI) lesions, and spinal cord involvement. However, due to the monophasic course in about half of the patients, long-term treatment is not recommended after the first clinical episode but is recommended for patients who experience relapse. Accurate and early diagnosis of MOGAD is essential for proper management and better outcome. This review covers the challenges in the diagnosis of MOGAD in children.

[Names] => Ünsal Yılmaz [CName] => [Doi] => 10.37349/ent.2024.00069 [Published] => February 27, 2024 [Viewed] => 593 [Downloaded] => 27 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00069 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 79 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:38–54 [Recommend] => 0 [Keywords] => Myelin oligodendrocyte glycoprotein antibody-associated disease, MOGAD, diagnosis [DetailTitle] => The Future of Biomarkers in CNS Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/79 [Id] => 100469 [ris] => https://www.explorationpub.com/uploads/Article/A100469/9c7717671bfbaf608823987b8e5c3b29.ris [bib] => https://www.explorationpub.com/uploads/Article/A100469/4c3a515988f535c24dee048547ce6358.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Yılmaz Ü. The diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in children. Explor Neuroprot Ther. 2024;4:38–54. https://doi.org/10.37349/ent.2024.00069 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-02-26 02:44:07 [Bib_Time] => 2024-02-26 02:44:07 [KeysWordContens] => The diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in children, Myelin oligodendrocyte glycoprotein antibody-associated disease, MOGAD, diagnosis, Over the last two decades, immunoglobulin G (IgG) antibodies against myelin oligodendrocyte glycoprotein (MOG), previously thought to be a biomarker of multiple sclerosis (MS), have been shown to cause a distinct disease called MOG antibody-associated disease (MOGAD). MOGAD accounts for approximately one-third of all demyelinating syndromes in children and is the second most common central nervous system (CNS) demyelinating disease after MS. The diagnosis is made by detecting anti-MOG IgG antibodies against the natural MOG antigen, in the presence of compatible clinical and neuroradiological features. However, due to controversies in the methodologies for detecting anti-MOG antibodies and their diagnostic cutoff values, as well as the expanding clinical spectrum, accurate diagnosis may be challenging, at least in a subset of patients. Clinical presentations of MOGAD vary by age; the highest rates are seen in acute disseminated encephalomyelitis in younger children and optic neuritis, myelitis, or brainstem symptoms in older children. Although it was previously thought to be a milder demyelinating disorder and to have a monophasic course in the majority of patients, recent studies have shown that relapses occur in about half of the patients and sequelae develop in a significant proportion of them, especially in those with persistently high antibody titers, leukodystrophy-like magnetic resonance imaging (MRI) lesions, and spinal cord involvement. However, due to the monophasic course in about half of the patients, long-term treatment is not recommended after the first clinical episode but is recommended for patients who experience relapse. Accurate and early diagnosis of MOGAD is essential for proper management and better outcome. This review covers the challenges in the diagnosis of MOGAD in children. ,Ünsal Yılmaz [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 1 [AuthorsName] => Ünsal Yılmaz ) [69] => Array ( [ArticleId] => 1138 [Create_Time] => 2024-02-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240227081318.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100470/100470.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100470/100470.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100470/100470_cover.png [JournalsId] => 7 [Title] => Advances in neuroprotective therapy for acute ischemic stroke [Abstract] => Acute ischemic stroke (AIS) is the leading cause of disability worldwide, and recanalization therapy is primary in the hyperacute phase of AIS. However, reperfusion injury and hemorrhagic transforma [AbstractComplete] =>

Acute ischemic stroke (AIS) is the leading cause of disability worldwide, and recanalization therapy is significant in the hyperacute phase of AIS. However, reperfusion injury and hemorrhagic transformation after recanalization predict poor prognosis of AIS. How to minimize reperfusion injury and hemorrhagic transformation, which greatly improves the prognosis of vascular recanalization, is becoming a hot topic in AIS research and an urgent problem to be solved. A wealth of neuroprotective drug studies is now available, while some of the neuroprotectants have met with failure in human studies. It is discussed in this review about the progress in neuroprotective therapy for AIS based on understanding the pathophysiologic mechanisms of reperfusion injury and hemorrhagic transformation, as well as challenges in exploring new neuroprotectants.

[Names] => Yang Yang ... Yi Li [CName] => [Doi] => 10.37349/ent.2024.00070 [Published] => February 27, 2024 [Viewed] => 764 [Downloaded] => 37 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00070 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 162 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:55–71 [Recommend] => 0 [Keywords] => Neuroprotective therapy, blood-brain barrier, acute ischemic stroke [DetailTitle] => Therapeutic Targets for Neuroprotection in Ischemic Stroke [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/162 [Id] => 100470 [ris] => https://www.explorationpub.com/uploads/Article/A100470/145d09c84cc4bf7aa990b98d709101bb.ris [bib] => https://www.explorationpub.com/uploads/Article/A100470/80178af19cd040c122acc705bb35d5b6.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Yang Y, Guo D, Liu Y, Li Y. Advances in neuroprotective therapy for acute ischemic stroke. Explor Neuroprot Ther. 2024;4:55–71. https://doi.org/10.37349/ent.2024.00070 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-02-26 01:07:55 [Bib_Time] => 2024-02-26 01:07:55 [KeysWordContens] => Advances in neuroprotective therapy for acute ischemic stroke, Neuroprotective therapy, blood-brain barrier, acute ischemic stroke, Acute ischemic stroke (AIS) is the leading cause of disability worldwide, and recanalization therapy is significant in the hyperacute phase of AIS. However, reperfusion injury and hemorrhagic transformation after recanalization predict poor prognosis of AIS. How to minimize reperfusion injury and hemorrhagic transformation, which greatly improves the prognosis of vascular recanalization, is becoming a hot topic in AIS research and an urgent problem to be solved. A wealth of neuroprotective drug studies is now available, while some of the neuroprotectants have met with failure in human studies. It is discussed in this review about the progress in neuroprotective therapy for AIS based on understanding the pathophysiologic mechanisms of reperfusion injury and hemorrhagic transformation, as well as challenges in exploring new neuroprotectants. ,Yang Yang ... Yi Li [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 1 [AuthorsName] => Yang Yang, Dandan Guo, Yiming Liu, Yi Li ) [70] => Array ( [ArticleId] => 1147 [Create_Time] => 2024-02-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240227094249.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100471/100471.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100471/100471.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100471/100471_cover.png [JournalsId] => 7 [Title] => Carbon nanotubes as neuroprotective agents [Abstract] => Carbon nanotubes, an emerging class of carbon nanomaterials, possess tremendous potential for application in biotechnology and biomedicine particularly in neurological disorders. Carbon nanotubes ow [AbstractComplete] =>

Carbon nanotubes, an emerging class of carbon nanomaterials, possess tremendous potential for application in biotechnology and biomedicine particularly in neurological disorders. Carbon nanotubes owing to their fascinating properties have the potential to revolutionize medicine and technology, particularly in the realm of drug delivery, biosensing, bioimaging, and as therapeutic agents to tackle complex neurological disorders such as Alzheimer’s and Parkinson’s disease. In this review, a summary of the use of carbon nanotubes for neuropathological outcomes such as alleviating oxidative stress and amyloid formation, which are well-studied molecular outcomes associated with Alzheimer’s and Parkinson’s disease. In the end, challenges associated with the clinical testing of carbon nanotubes and possible ways to overcome them are highlighted.

[Names] => Daisy L. Wilson ... Mahesh Narayan [CName] => [Doi] => 10.37349/ent.2024.00071 [Published] => February 27, 2024 [Viewed] => 582 [Downloaded] => 25 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00071 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 118 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:72–81 [Recommend] => 0 [Keywords] => Carbon nanotubes, carbon nanomaterials, oxidative stress, amyloid fibrils, neurodegenerative disorders [DetailTitle] => Parkinson's Disease: Principal Targets and Interventional Mechanisms [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/118 [Id] => 100471 [ris] => https://www.explorationpub.com/uploads/Article/A100471/cc4831afa4a82670e32ef455fa3cdc27.ris [bib] => https://www.explorationpub.com/uploads/Article/A100471/4046bd8db90f73408ef161f9db2d7453.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Wilson DL, Ahlawat J, Narayan M. Carbon nanotubes as neuroprotective agents. Explor Neuroprot Ther. 2024;4:72–81. https://doi.org/10.37349/ent.2024.00071 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-02-27 03:00:37 [Bib_Time] => 2024-02-27 09:36:03 [KeysWordContens] => Carbon nanotubes as neuroprotective agents, Carbon nanotubes, carbon nanomaterials, oxidative stress, amyloid fibrils, neurodegenerative disorders, Carbon nanotubes, an emerging class of carbon nanomaterials, possess tremendous potential for application in biotechnology and biomedicine particularly in neurological disorders. Carbon nanotubes owing to their fascinating properties have the potential to revolutionize medicine and technology, particularly in the realm of drug delivery, biosensing, bioimaging, and as therapeutic agents to tackle complex neurological disorders such as Alzheimer’s and Parkinson’s disease. In this review, a summary of the use of carbon nanotubes for neuropathological outcomes such as alleviating oxidative stress and amyloid formation, which are well-studied molecular outcomes associated with Alzheimer’s and Parkinson’s disease. In the end, challenges associated with the clinical testing of carbon nanotubes and possible ways to overcome them are highlighted. ,Daisy L. Wilson ... Mahesh Narayan [PublishedText] => Published [IsEdit] => 0 [AccountId] => 21 [Zh] => 1 [AuthorsName] => Daisy L. Wilson, Jyoti Ahlawat, Mahesh Narayan ) [71] => Array ( [ArticleId] => 1164 [Create_Time] => 2024-02-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240228013157.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100472/100472.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100472/100472.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100472/100472_cover.png [JournalsId] => 7 [Title] => Analysis of congenital Zika syndrome clinicopathologic findings reported in the 8 years since the Brazilian outbreak [Abstract] => Aim: A Zika virus outbreak that began in Brazil, developed into an international public health emergency that extended from February 2015 until November 2016. Zika-infected pregnant women gave bi [AbstractComplete] =>

Aim:

A Zika virus outbreak that began in Brazil, developed into an international public health emergency that extended from February 2015 until November 2016. Zika-infected pregnant women gave birth to a cohort of infants with congenital Zika syndrome (CZS) originally defined by severe microcephaly, retinal scarring, joint deformities, and hypertonia. This study examines the nature, extent, and severity of all CZS clinicopathologic findings described to date, compiled and analyzed by system. It reviews studies monitoring disease progression and proposing classification schemes for CZS stages. The teratogenic cellular and molecular mechanisms implicated in CZS pathogenesis are also discussed.

Methods:

A systematic review was conducted by literature search through WorldCat.org and ProQuest Central databases to identify studies on case series from the 2015–2016 CZS outbreak.

Results:

Twenty-six reports were included describing radiologic, ophthalmologic, audiologic, orthopedic, and laboratory test results in CZS cases including stillborns between 2016 and 2023. CZS neuropathology included prenatal and postnatal microcephaly, cerebral calcifications, quadriparesis, epilepsy, ventriculomegaly, reduced cerebral parenchyma, malformation of cortical development, and sleep electroencephalogram disturbances. Visual deficits were due to retinal and optic nerve lesions. Conductive and sensorineural hearing deficits were stable. Hypertonia, hypotonia, and spasticity with foot, hip, knee, and shoulder deformities resulted in arthrogryposis and restricted joint mobility. There was enlargement of immune organs, increased leukocyte counts, and cytokine dysregulation. Oro-craniofacial deformities affected the midface and caused dental eruption delay. Additional studies proposed that these systemic teratogenic effects could be attributable to transplacental Zika virus infection of multiple fetal progenitor cell lineages.

Conclusions:

The CZS-associated impairments in brain, eye, musculoskeletal, and immunologic functions caused disabilities that varied from moderate to severe, and significantly increased age-specific mortality rates. Further research is warranted to assess progression, classify stages, elucidate the precise molecular mechanisms mediating Zika teratogenicity, develop suitable therapeutic strategies, and design supportive social policies.

[Names] => Dhaara Shah ... Rana Zeine [CName] => [Doi] => 10.37349/ent.2024.00072 [Published] => February 27, 2024 [Viewed] => 1245 [Downloaded] => 31 [Subject] => Systematic Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00072 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 224 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:82–99 [Recommend] => 0 [Keywords] => Congenital Zika syndrome, teratogenic, microcephaly, cerebral palsy, epilepsy, craniofacial, arthrogryposis, immune dysregulation [DetailTitle] => Neuro-Inflammation as a Target in the Design of Multifunctional Drug Candidates for Neurodegenerative Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/224 [Id] => 100472 [ris] => https://www.explorationpub.com/uploads/Article/A100472/7a64829723035b5dc7b89d06e678ff66.ris [bib] => https://www.explorationpub.com/uploads/Article/A100472/2334515407dad217c268f05150ef2a9d.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Shah D, Shah D, Mua O, Zeine R. Analysis of congenital Zika syndrome clinicopathologic findings reported in the 8 years since the Brazilian outbreak. Explor Neuroprot Ther. 2024;4:82–99. https://doi.org/10.37349/ent.2024.00072 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-02-27 05:03:35 [Bib_Time] => 2024-02-27 05:03:35 [KeysWordContens] => Analysis of congenital Zika syndrome clinicopathologic findings reported in the 8 years since the Brazilian outbreak, Congenital Zika syndrome, teratogenic, microcephaly, cerebral palsy, epilepsy, craniofacial, arthrogryposis, immune dysregulation, Aim: A Zika virus outbreak that began in Brazil, developed into an international public health emergency that extended from February 2015 until November 2016. Zika-infected pregnant women gave birth to a cohort of infants with congenital Zika syndrome (CZS) originally defined by severe microcephaly, retinal scarring, joint deformities, and hypertonia. This study examines the nature, extent, and severity of all CZS clinicopathologic findings described to date, compiled and analyzed by system. It reviews studies monitoring disease progression and proposing classification schemes for CZS stages. The teratogenic cellular and molecular mechanisms implicated in CZS pathogenesis are also discussed. Methods: A systematic review was conducted by literature search through WorldCat.org and ProQuest Central databases to identify studies on case series from the 2015–2016 CZS outbreak. Results: Twenty-six reports were included describing radiologic, ophthalmologic, audiologic, orthopedic, and laboratory test results in CZS cases including stillborns between 2016 and 2023. CZS neuropathology included prenatal and postnatal microcephaly, cerebral calcifications, quadriparesis, epilepsy, ventriculomegaly, reduced cerebral parenchyma, malformation of cortical development, and sleep electroencephalogram disturbances. Visual deficits were due to retinal and optic nerve lesions. Conductive and sensorineural hearing deficits were stable. Hypertonia, hypotonia, and spasticity with foot, hip, knee, and shoulder deformities resulted in arthrogryposis and restricted joint mobility. There was enlargement of immune organs, increased leukocyte counts, and cytokine dysregulation. Oro-craniofacial deformities affected the midface and caused dental eruption delay. Additional studies proposed that these systemic teratogenic effects could be attributable to transplacental Zika virus infection of multiple fetal progenitor cell lineages. Conclusions: The CZS-associated impairments in brain, eye, musculoskeletal, and immunologic functions caused disabilities that varied from moderate to severe, and significantly increased age-specific mortality rates. Further research is warranted to assess progression, classify stages, elucidate the precise molecular mechanisms mediating Zika teratogenicity, develop suitable therapeutic strategies, and design supportive social policies. ,Dhaara Shah ... Rana Zeine [PublishedText] => Published [IsEdit] => 0 [AccountId] => 78 [Zh] => 1 [AuthorsName] => Dhaara Shah, Dhairavi Shah, Olivia Mua, Rana Zeine ) [72] => Array ( [ArticleId] => 1179 [Create_Time] => 2024-03-19 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240408072903.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100473/100473.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100473/100473.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100473/100473_cover.png [JournalsId] => 7 [Title] => Targeting short-chain fatty acids receptors signalling for neurological disorders treatment [Abstract] => Short-chain fatty acids (SCFAs) play a key role regulating immune and metabolic homeostasis. Consequently, dysregulation in SCFA levels is involved in the pathogenesis of autoimmune, inflammatory, m [AbstractComplete] =>

Short-chain fatty acids (SCFAs) play a key role regulating immune and metabolic homeostasis. Consequently, dysregulation in SCFA levels is involved in the pathogenesis of autoimmune, inflammatory, metabolic, and neurodegenerative disorders. These metabolites are generated by gut microbiota, and their production is influenced mainly by diet. Here, an overview is provided of how SCFA production is associated with diet and with neurological disorders. The mechanisms by which SCFAs exert beneficial effects are analysed, along with how their production may be boosted by diet and how the use of specific dietary interventions might improve the outcome of neurological diseases.

[Names] => Carolina Prado, Rodrigo Pacheco [CName] => [Doi] => 10.37349/ent.2024.00073 [Published] => March 19, 2024 [Viewed] => 513 [Downloaded] => 29 [Subject] => Perspective [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00073 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:100–107 [Recommend] => 0 [Keywords] => Short-chain fatty acids, autoimmunity, microbiota, gut-brain axis [DetailTitle] => [DetailUrl] => [Id] => 100473 [ris] => https://www.explorationpub.com/uploads/Article/A100473/ca693fc90fe93c1e2f4f7db0f2f2fd7f.ris [bib] => https://www.explorationpub.com/uploads/Article/A100473/3afb5843f5537c2ca94916526c591fb7.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Prado C, Pacheco R. Targeting short-chain fatty acids receptors signalling for neurological disorders treatment. Explor Neuroprot Ther. 2024;4:100–7. https://doi.org/10.37349/ent.2024.00073 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-03-15 09:13:24 [Bib_Time] => 2024-03-15 09:13:24 [KeysWordContens] => Targeting short-chain fatty acids receptors signalling for neurological disorders treatment, Short-chain fatty acids, autoimmunity, microbiota, gut-brain axis, Short-chain fatty acids (SCFAs) play a key role regulating immune and metabolic homeostasis. Consequently, dysregulation in SCFA levels is involved in the pathogenesis of autoimmune, inflammatory, metabolic, and neurodegenerative disorders. These metabolites are generated by gut microbiota, and their production is influenced mainly by diet. Here, an overview is provided of how SCFA production is associated with diet and with neurological disorders. The mechanisms by which SCFAs exert beneficial effects are analysed, along with how their production may be boosted by diet and how the use of specific dietary interventions might improve the outcome of neurological diseases. ,Carolina Prado, Rodrigo Pacheco [PublishedText] => Published [IsEdit] => 0 [AccountId] => 78 [Zh] => 1 [AuthorsName] => Carolina Prado, Rodrigo Pacheco ) [73] => Array ( [ArticleId] => 1208 [Create_Time] => 2024-04-07 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240426054217.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100474/100474.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100474/100474.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100474/100474_cover.png [JournalsId] => 7 [Title] => “Vitaction” deficiency: a possible root cause for multiple lifestyle disorders including Alzheimer’s disease [Abstract] => Behavioural environment and behavioural responses of an individual are known to affect multiple aspects of physiology including neuroendocrine and growth factor signalling, angiogenesis, stem cell d [AbstractComplete] =>

Behavioural environment and behavioural responses of an individual are known to affect multiple aspects of physiology including neuroendocrine and growth factor signalling, angiogenesis, stem cell dynamics, tissue homeostasis, and maintenance. Despite substantial evidence, the role of behaviour-physiology interface in human health and disease remains underappreciated. The hypothesis proposed here suggests that deficiencies of certain behaviours that have evolved to become essential or “vitactions” can potentially trigger multiple health problems. Altered growth factor expression because of vitaction deficiencies affects angiogenesis and vascular function, neuronal maintenance, transport of glucose and other nutrients to the brain, mitochondrial function, oxidative stress, inflammation, and protein aggregation dynamics all implicated in Alzheimer’s disease (AD). Exercise is already known to be effective in prevention of AD. The hypothesis suggests that it is the behavioural component of exercise over mechanical activity and calorie burning that has crucial effects on brain health through multiple signalling pathways. Similar to vitamin deficiencies, where supplying the deficient vitamin is the only effective solution, for vitaction deficiencies supplying the deficient behavioural stimuli through behaviourally enriched exercise can be the most effective remedy.

[Names] => Milind Watve, Ashwini Keskar Sardeshmukh [CName] => [Doi] => 10.37349/ent.2024.00074 [Published] => April 07, 2024 [Viewed] => 642 [Downloaded] => 23 [Subject] => Perspective [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00074 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 135 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:108–118 [Recommend] => 0 [Keywords] => Evolutionary medicine, mismatch hypotheses, growth factor signalling, angiogenesis, Alzheimer’s disease [DetailTitle] => The Urgent Need for New Hypotheses to Develop Effective Therapeutic Tools Against Alzheimer's Disease [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/135 [Id] => 100474 [ris] => https://www.explorationpub.com/uploads/Article/A100474/09f2d408300852e6fe8532f675134f87.ris [bib] => https://www.explorationpub.com/uploads/Article/A100474/f76d90368272d8d730f95420861eba98.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Watve M, Keskar Sardeshmukh A. “Vitaction” deficiency: a possible root cause for multiple lifestyle disorders including Alzheimer’s disease. Explor Neuroprot Ther. 2024;4:108–18. https://doi.org/ent.2024.00074 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-04-07 07:19:06 [Bib_Time] => 2024-04-07 07:19:06 [KeysWordContens] => “Vitaction” deficiency: a possible root cause for multiple lifestyle disorders including Alzheimer’s disease, Evolutionary medicine, mismatch hypotheses, growth factor signalling, angiogenesis, Alzheimer’s disease, Behavioural environment and behavioural responses of an individual are known to affect multiple aspects of physiology including neuroendocrine and growth factor signalling, angiogenesis, stem cell dynamics, tissue homeostasis, and maintenance. Despite substantial evidence, the role of behaviour-physiology interface in human health and disease remains underappreciated. The hypothesis proposed here suggests that deficiencies of certain behaviours that have evolved to become essential or “vitactions” can potentially trigger multiple health problems. Altered growth factor expression because of vitaction deficiencies affects angiogenesis and vascular function, neuronal maintenance, transport of glucose and other nutrients to the brain, mitochondrial function, oxidative stress, inflammation, and protein aggregation dynamics all implicated in Alzheimer’s disease (AD). Exercise is already known to be effective in prevention of AD. The hypothesis suggests that it is the behavioural component of exercise over mechanical activity and calorie burning that has crucial effects on brain health through multiple signalling pathways. Similar to vitamin deficiencies, where supplying the deficient vitamin is the only effective solution, for vitaction deficiencies supplying the deficient behavioural stimuli through behaviourally enriched exercise can be the most effective remedy. ,Milind Watve, Ashwini Keskar Sardeshmukh [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 1 [AuthorsName] => Milind Watve, Ashwini Keskar Sardeshmukh ) [74] => Array ( [ArticleId] => 1227 [Create_Time] => 2024-04-16 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240416070050.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100475/100475.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100475/100475.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100475/100475_cover.png [JournalsId] => 7 [Title] => Biomarkers in neurodegenerative diseases: a broad overview [Abstract] => Degeneration and dysfunction of neurons in the brain are hallmarks of neurodegenerative diseases. Over the past decades, significant efforts have been devoted to the development and validation of bi [AbstractComplete] =>

Degeneration and dysfunction of neurons in the brain are hallmarks of neurodegenerative diseases. Over the past decades, significant efforts have been devoted to the development and validation of biomarkers for neurodegenerative diseases. The range and diversity of biomarkers for central nervous system (CNS) diseases has continued to expand, encompassing biofluid-based sources such as blood or cerebrospinal fluid (CSF), nucleic acids, tissues, and imaging. While imaging and tissue biopsy-based markers are continually being identified and their applications expanding, they do have limitations compared with RNA and protein biomarkers. This review comprehensively summarizes various biomarkers, including microRNA (miRNA), long noncoding RNA (lncRNA), circulating miRNA (cimiRNA), and proteins, in the context of CNS disorders. In addition, the review emphasizes the existing limitations and challenges associated with the use of biomarkers in both clinical practice and research on neurodegenerative diseases. In conclusion, this review provides an insightful overview of the identified biomarkers for neurodegenerative diseases, underscoring the crucial role of biomarker research in combating these debilitating conditions. The article also highlights future challenges related to the implementation of novel biomarkers in clinical practice and trials, thereby contributing to the ongoing efforts to advance the understanding and management of neurodegenerative diseases.

[Names] => Sathish Selvam, Velpandi Ayyavoo [CName] => [Doi] => 10.37349/ent.2024.00075 [Published] => April 16, 2024 [Viewed] => 967 [Downloaded] => 33 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00075 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 79 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:119–147 [Recommend] => 0 [Keywords] => Central nervous system, biomarkers, miRNA, proteins, amyloid-beta 42/40, neurological disorders [DetailTitle] => The Future of Biomarkers in CNS Diseases [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/79 [Id] => 100475 [ris] => https://www.explorationpub.com/uploads/Article/A100475/396a1393f0c840d18897ae05f54d8f3f.ris [bib] => https://www.explorationpub.com/uploads/Article/A100475/806a1cdb081f0870fec465aaf27ad4ce.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Selvam S, Ayyavoo V. Biomarkers in neurodegenerative diseases: a broad overview. Explor Neuroprot Ther. 2024;4:119–47. https://doi.org/10.37349/ent.2024.00075 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-04-16 01:42:38 [Bib_Time] => 2024-04-16 01:42:38 [KeysWordContens] => Biomarkers in neurodegenerative diseases: a broad overview, Central nervous system, biomarkers, miRNA, proteins, amyloid-beta 42/40, neurological disorders, Degeneration and dysfunction of neurons in the brain are hallmarks of neurodegenerative diseases. Over the past decades, significant efforts have been devoted to the development and validation of biomarkers for neurodegenerative diseases. The range and diversity of biomarkers for central nervous system (CNS) diseases has continued to expand, encompassing biofluid-based sources such as blood or cerebrospinal fluid (CSF), nucleic acids, tissues, and imaging. While imaging and tissue biopsy-based markers are continually being identified and their applications expanding, they do have limitations compared with RNA and protein biomarkers. This review comprehensively summarizes various biomarkers, including microRNA (miRNA), long noncoding RNA (lncRNA), circulating miRNA (cimiRNA), and proteins, in the context of CNS disorders. In addition, the review emphasizes the existing limitations and challenges associated with the use of biomarkers in both clinical practice and research on neurodegenerative diseases. In conclusion, this review provides an insightful overview of the identified biomarkers for neurodegenerative diseases, underscoring the crucial role of biomarker research in combating these debilitating conditions. The article also highlights future challenges related to the implementation of novel biomarkers in clinical practice and trials, thereby contributing to the ongoing efforts to advance the understanding and management of neurodegenerative diseases. ,Sathish Selvam, Velpandi Ayyavoo [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 0 [AuthorsName] => Sathish Selvam, Velpandi Ayyavoo ) [75] => Array ( [ArticleId] => 1245 [Create_Time] => 2024-04-18 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240418015048.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100476/100476.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100476/100476.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100476/100476_cover.png [JournalsId] => 7 [Title] => Neuronal plasticity in dorsal root ganglia following sciatic nerve injury [Abstract] => It is widely known that each tissue has unique mechanisms to respond to injury and maintain homeostasis effectively. Although peripheral nerves have limited regeneration capacity, they conduct a com [AbstractComplete] =>

It is widely known that each tissue has unique mechanisms to respond to injury and maintain homeostasis effectively. Although peripheral nerves have limited regeneration capacity, they conduct a complicated regeneration process by orchestrating multiple cell complexes after injury. In addition to drawing attention to anterograde and retrograde transportation, the absence of a cell body in the damaged area also points to the significance of immune and glial cells in the environment. Cellular reorganization following injury in the dorsal root ganglion, which takes place in the cell bodies of sensory peripheral nerve fibers, has attracted much attention. Growing research has been focused on investigating the molecular and cellular interactions occurring in sensory neurons and glial cells within the dorsal root ganglia after injury. It is clearly becoming that the sensory neurons and glial cells in the dorsal root ganglion are derived from the same embryological origins. Therefore, this information attracts attention to the potential of these two cells to differentiate into each other in case of injury. The focus of these studies is to illuminate the genes and pathways responsible for an increase in the plasticity of the neurogenic cell line following nerve injury. This review explores and discusses the underlying mechanisms responsible for maintaining homeostasis in the dorsal root ganglion and regeneration of peripheral nerves and how neuronal plasticity functions in the regeneration of the injury.

[Names] => Burcu Delibaş ... Süleyman Kaplan [CName] => [Doi] => 10.37349/ent.2024.00076 [Published] => April 17, 2024 [Viewed] => 327 [Downloaded] => 26 [Subject] => Mini Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00076 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 117 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:148–157 [Recommend] => 0 [Keywords] => Dorsal root ganglia, neuronal plasticity, sciatic nerve injury, rat [DetailTitle] => Peripheral Nerve Regeneration [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/117 [Id] => 100476 [ris] => https://www.explorationpub.com/uploads/Article/A100476/9d03692b27175fa2a07c8d203560d540.ris [bib] => https://www.explorationpub.com/uploads/Article/A100476/8681618deec725490ffc158b447a468e.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Delibaş B, Elamin AAE, Kaplan S. Neuronal plasticity in dorsal root ganglia following sciatic nerve injury. Explor Neuroprot Ther. 2024;4:148–57. https://doi.org/10.37349/ent.2024.00076 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-04-17 08:16:58 [Bib_Time] => 2024-04-17 08:16:58 [KeysWordContens] => Neuronal plasticity in dorsal root ganglia following sciatic nerve injury, Dorsal root ganglia, neuronal plasticity, sciatic nerve injury, rat, It is widely known that each tissue has unique mechanisms to respond to injury and maintain homeostasis effectively. Although peripheral nerves have limited regeneration capacity, they conduct a complicated regeneration process by orchestrating multiple cell complexes after injury. In addition to drawing attention to anterograde and retrograde transportation, the absence of a cell body in the damaged area also points to the significance of immune and glial cells in the environment. Cellular reorganization following injury in the dorsal root ganglion, which takes place in the cell bodies of sensory peripheral nerve fibers, has attracted much attention. Growing research has been focused on investigating the molecular and cellular interactions occurring in sensory neurons and glial cells within the dorsal root ganglia after injury. It is clearly becoming that the sensory neurons and glial cells in the dorsal root ganglion are derived from the same embryological origins. Therefore, this information attracts attention to the potential of these two cells to differentiate into each other in case of injury. The focus of these studies is to illuminate the genes and pathways responsible for an increase in the plasticity of the neurogenic cell line following nerve injury. This review explores and discusses the underlying mechanisms responsible for maintaining homeostasis in the dorsal root ganglion and regeneration of peripheral nerves and how neuronal plasticity functions in the regeneration of the injury. ,Burcu Delibaş ... Süleyman Kaplan [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 0 [AuthorsName] => Burcu Delibaş, Abdalla Ahmed Eldaw Elamin, Süleyman Kaplan ) [76] => Array ( [ArticleId] => 1254 [Create_Time] => 2024-04-22 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240422050252.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100477/100477.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100477/100477.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100477/100477_cover.png [JournalsId] => 7 [Title] => Lifetime stressors relate to invisible symptoms of multiple sclerosis [Abstract] => Aim: Childhood stressors can increase adult stress perception and may accumulate over the lifespan to impact symptoms of multiple sclerosis (MS). Growing evidence links childhood stressors (e.g., [AbstractComplete] =>

Aim:

Childhood stressors can increase adult stress perception and may accumulate over the lifespan to impact symptoms of multiple sclerosis (MS). Growing evidence links childhood stressors (e.g., abuse, neglect) to fatigue, pain, and psychiatric morbidity in adults with MS; yet literature in this area is lacking a comprehensive lifespan approach. The aim of this cross-sectional study was to examine contributions of childhood and adulthood stressor characteristics (i.e., count, severity), on three individual outcomes: fatigue, pain interference, and psychiatric morbidity in People with MS (PwMS).

Methods:

An online survey was distributed through the National MS Society. Hierarchical block regression modeling was used to sequentially assess baseline demographics, childhood stressors, and adult stressors per outcome. We hypothesized that child and adult stressors would significantly contribute to fatigue, pain interference, and psychiatric morbidity.

Results:

Overall, 713 PwMS informed at least one final analytic model. Both childhood and adult stressors significantly contributed to pain interference and psychiatric morbidity. Adult stressor severity independently correlated with psychiatric morbidity (P < 0.0001). Childhood stressors significantly contributed to fatigue (LR test P < 0.0001). Childhood stressor severity independently significantly correlated with both fatigue likelihood (P = 0.03) and magnitude (P < 0.001).

Conclusions:

This work supports a relationship between stressors across the lifespan and fatigue, pain, and psychiatric morbidity in PwMS. Stressor severity may have an important role which may not be captured in count-based trauma measurement tools. Clinicians and researchers should consider lifetime stress when addressing fatigue, pain, and psychiatric morbidity among PwMS.

[Names] => Carri S. Polick ... Sarah A. Stoddard [CName] => [Doi] => 10.37349/ent.2024.00077 [Published] => April 22, 2024 [Viewed] => 433 [Downloaded] => 22 [Subject] => Original Article [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00077 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:158–171 [Recommend] => 0 [Keywords] => Adverse childhood experiences, stressors, multiple sclerosis, fatigue, pain, psychiatric morbidity [DetailTitle] => [DetailUrl] => [Id] => 100477 [ris] => https://www.explorationpub.com/uploads/Article/A100477/f8092d4c691d2d070d4437a97b064661.ris [bib] => https://www.explorationpub.com/uploads/Article/A100477/e11cbc1f9030e6286b8cff8ccb71fb3a.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Polick CS, Braley TJ, Ploutz-Snyder R, Connell CM, Watson A, Stoddard SA. Lifetime stressors relate to invisible symptoms of multiple sclerosis. Explor Neuroprot Ther. 2024;4:158–71. https://doi.org/10.37349/ent.2024.00077 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-04-19 01:34:42 [Bib_Time] => 2024-04-19 01:34:42 [KeysWordContens] => Lifetime stressors relate to invisible symptoms of multiple sclerosis, Adverse childhood experiences, stressors, multiple sclerosis, fatigue, pain, psychiatric morbidity, Aim: Childhood stressors can increase adult stress perception and may accumulate over the lifespan to impact symptoms of multiple sclerosis (MS). Growing evidence links childhood stressors (e.g., abuse, neglect) to fatigue, pain, and psychiatric morbidity in adults with MS; yet literature in this area is lacking a comprehensive lifespan approach. The aim of this cross-sectional study was to examine contributions of childhood and adulthood stressor characteristics (i.e., count, severity), on three individual outcomes: fatigue, pain interference, and psychiatric morbidity in People with MS (PwMS). Methods: An online survey was distributed through the National MS Society. Hierarchical block regression modeling was used to sequentially assess baseline demographics, childhood stressors, and adult stressors per outcome. We hypothesized that child and adult stressors would significantly contribute to fatigue, pain interference, and psychiatric morbidity. Results: Overall, 713 PwMS informed at least one final analytic model. Both childhood and adult stressors significantly contributed to pain interference and psychiatric morbidity. Adult stressor severity independently correlated with psychiatric morbidity (P < 0.0001). Childhood stressors significantly contributed to fatigue (LR test P < 0.0001). Childhood stressor severity independently significantly correlated with both fatigue likelihood (P = 0.03) and magnitude (P < 0.001). Conclusions: This work supports a relationship between stressors across the lifespan and fatigue, pain, and psychiatric morbidity in PwMS. Stressor severity may have an important role which may not be captured in count-based trauma measurement tools. Clinicians and researchers should consider lifetime stress when addressing fatigue, pain, and psychiatric morbidity among PwMS. ,Carri S. Polick ... Sarah A. Stoddard [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 0 [AuthorsName] => Carri S. Polick, Tiffany J. Braley, Robert Ploutz-Snyder, Cathleen M. Connell, Ali Watson, Sarah A. Stoddard ) [77] => Array ( [ArticleId] => 1262 [Create_Time] => 2024-04-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240426045914.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100478/100478.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100478/100478.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100478/100478_cover.png [JournalsId] => 7 [Title] => Cerebral stroke-induced neurogenesis: insights and therapeutic implications [Abstract] => Stroke, one of the leading causes of global morbidity and mortality, results from disrupted cerebral blood circulation, leads to cellular damage or death. Ischemic stroke, the predominant subtype, r [AbstractComplete] =>

Stroke, one of the leading causes of global morbidity and mortality, results from disrupted cerebral blood circulation, leads to cellular damage or death. Ischemic stroke, the predominant subtype, relies mainly on recombinant tissue plasminogen activator (rtPA) and endovascular thrombectomy for the treatment. Neurological impairments following ischemic stroke highlight the importance of understanding the interplay between neuroinflammation and neurogenesis in brain repair. Research reveals a complex relationship, where inflammation both promotes and hinders neurogenesis, impacting post-stroke outcomes. The subventricular zone (SVZ) of striatum and sub granular zone (SGZ) in hippocampus play pivotal roles in adult neurogenesis, with distinct characteristics and functions. SVZ neurogenesis involves neuroblast progenitors migrating to the olfactory bulb, while SGZ facilitates granule cell generation for hippocampal function. Understanding the intricate processes of neuroinflammation, neurogenesis, and angiogenesis is crucial for developing effective stroke therapeutics. Promising avenues include drug therapy, selective serotonin reuptake inhibitors, antibody therapy, angiogenesis stimulation, growth factor therapy, hormone therapy, miRNAs, extracellular vesicles, and neuroprotective agents. Stem cell therapy, exploring various cell types, holds potential for neuronal replacement and recovery. In conclusion, deciphering the roles of SVZ and SGZ in neurogenesis, unraveling the complexity of neuroinflammation’s impact on repair, and exploring diverse therapeutic approaches highlight the need for comprehensive investigations to enhance stroke outcomes. The multifaceted landscape of stroke therapeutics presents challenges, but ongoing research offers promising avenues for bridging the gap between preclinical findings and clinical treatments.

[Names] => Mydhili Radhakrishnan ... Sumana Chakravarty [CName] => [Doi] => 10.37349/ent.2024.00078 [Published] => April 26, 2024 [Viewed] => 380 [Downloaded] => 27 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00078 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 55 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:172–197 [Recommend] => 0 [Keywords] => Neurogenesis, cerebral ischemia, neuroinflammation, therapeutics [DetailTitle] => Intervention of Neuroimmune Responses [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/55 [Id] => 100478 [ris] => https://www.explorationpub.com/uploads/Article/A100478/46d182191e359945f3266f181015fa9d.ris [bib] => https://www.explorationpub.com/uploads/Article/A100478/5d2e0b2335188a943ccefa485d2639ad.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Radhakrishnan M, Kushwaha R, Acharya BS, Kumar A, Chakravarty S. Cerebral stroke-induced neurogenesis: insights and therapeutic implications. Explor Neuroprot Ther. 2024;4:172–97. https://doi.org/10.37349/ent.2024.00078 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-04-25 03:12:52 [Bib_Time] => 2024-04-25 03:12:52 [KeysWordContens] => Cerebral stroke-induced neurogenesis: insights and therapeutic implications, Neurogenesis, cerebral ischemia, neuroinflammation, therapeutics, Stroke, one of the leading causes of global morbidity and mortality, results from disrupted cerebral blood circulation, leads to cellular damage or death. Ischemic stroke, the predominant subtype, relies mainly on recombinant tissue plasminogen activator (rtPA) and endovascular thrombectomy for the treatment. Neurological impairments following ischemic stroke highlight the importance of understanding the interplay between neuroinflammation and neurogenesis in brain repair. Research reveals a complex relationship, where inflammation both promotes and hinders neurogenesis, impacting post-stroke outcomes. The subventricular zone (SVZ) of striatum and sub granular zone (SGZ) in hippocampus play pivotal roles in adult neurogenesis, with distinct characteristics and functions. SVZ neurogenesis involves neuroblast progenitors migrating to the olfactory bulb, while SGZ facilitates granule cell generation for hippocampal function. Understanding the intricate processes of neuroinflammation, neurogenesis, and angiogenesis is crucial for developing effective stroke therapeutics. Promising avenues include drug therapy, selective serotonin reuptake inhibitors, antibody therapy, angiogenesis stimulation, growth factor therapy, hormone therapy, miRNAs, extracellular vesicles, and neuroprotective agents. Stem cell therapy, exploring various cell types, holds potential for neuronal replacement and recovery. In conclusion, deciphering the roles of SVZ and SGZ in neurogenesis, unraveling the complexity of neuroinflammation’s impact on repair, and exploring diverse therapeutic approaches highlight the need for comprehensive investigations to enhance stroke outcomes. The multifaceted landscape of stroke therapeutics presents challenges, but ongoing research offers promising avenues for bridging the gap between preclinical findings and clinical treatments. ,Mydhili Radhakrishnan ... Sumana Chakravarty [PublishedText] => Published [IsEdit] => 0 [AccountId] => 78 [Zh] => 0 [AuthorsName] => Mydhili Radhakrishnan, Roli Kushwaha, B. Supraja Acharya, Arvind Kumar, Sumana Chakravarty ) [78] => Array ( [ArticleId] => 1280 [Create_Time] => 2024-05-16 [zipUrl] => https://www.explorationpub.com/uploads/zip/202405/20240515080507.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100479/100479.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100479/100479.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100479/100479_cover.png [JournalsId] => 7 [Title] => Diverse avenues of research support the transmethylation theory of psychosis: implications for neuroprotection [Abstract] => Transmethylation in the context of psychiatry has historically referred to the enzymatic transfer of a methyl group from one biochemical to another, whose resulting function can change so dramatical [AbstractComplete] =>

Transmethylation in the context of psychiatry has historically referred to the enzymatic transfer of a methyl group from one biochemical to another, whose resulting function can change so dramatically that a biochemical like tryptamine, for example, is converted into the hallucinogen dimethyltryptamine. Central to endogenous methylation activity is the folate cycle, which generates the primary transferable methyl groups in mammalian biochemistry. The relevance of this cycle to mental health becomes clear when the cycle is dysregulated, often leading to a buildup of both homocysteine and S-adenosylhomocysteine (SAH), while accompanied by a transient reduction in the intended physiologic target, S-adenosylmethionine (SAM). This paper includes an in-depth review of the causes of folate cycle perturbations associated with psychotic symptoms, expounding on alternative downstream pathways which are activated and pointing toward potential etiologic agents of the associated psychosis, the methylated tertiary amines N-methyl-salsolinol, N-methyl-norsalsolinol, and adrenochrome, which appear in scientific reports concerning their association with hallucinogenic and/or neurotoxic outcomes. Electrotopological state (E-state) data has been generated for these compounds, illustrating a strong similarity with hallucinogens, particularly in terms of the E-state of the nitrogen in their tertiary amine moieties. In light of the role the folate cycle plays in transmethylation, neuroprotective strategies to prevent the transition to psychosis are suggested, including the advisory that folate supplementation can be harmful depending on the status of other relevant biochemicals.

[Names] => Christine L. Miller [CName] => [Doi] => 10.37349/ent.2024.00079 [Published] => May 15, 2024 [Viewed] => 137 [Downloaded] => 9 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00079 [Inline] => 1 [Type] => 0 [Issue] => [Topic] => 228 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:198–239 [Recommend] => 0 [Keywords] => hallucinogens, psychotic disorders, folate cycle, homocysteine, vitamin B12, Folfirinox, MTHFR, electrotopology [DetailTitle] => Defending the Brain and the Mind: Exploring Neuroprotective Therapies for Mental Health Disorders [DetailUrl] => https://www.explorationpub.com/Journals/ent/Special_Issues/228 [Id] => 100479 [ris] => https://www.explorationpub.com/uploads/Article/A100479/4994c57bff35fdc918e4b13dd54da2a8.ris [bib] => https://www.explorationpub.com/uploads/Article/A100479/25f10161b47928ac3e50dee0ead77357.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Miller CL. Diverse avenues of research support the transmethylation theory of psychosis: implications for neuroprotection. Explor Neuroprot Ther. 2024;4:198–239. https://doi.org/10.37349/ent.2024.00079 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-05-13 09:14:31 [Bib_Time] => 2024-05-13 09:14:31 [KeysWordContens] => Diverse avenues of research support the transmethylation theory of psychosis: implications for neuroprotection, hallucinogens, psychotic disorders, folate cycle, homocysteine, vitamin B12, Folfirinox, MTHFR, electrotopology, Transmethylation in the context of psychiatry has historically referred to the enzymatic transfer of a methyl group from one biochemical to another, whose resulting function can change so dramatically that a biochemical like tryptamine, for example, is converted into the hallucinogen dimethyltryptamine. Central to endogenous methylation activity is the folate cycle, which generates the primary transferable methyl groups in mammalian biochemistry. The relevance of this cycle to mental health becomes clear when the cycle is dysregulated, often leading to a buildup of both homocysteine and S-adenosylhomocysteine (SAH), while accompanied by a transient reduction in the intended physiologic target, S-adenosylmethionine (SAM). This paper includes an in-depth review of the causes of folate cycle perturbations associated with psychotic symptoms, expounding on alternative downstream pathways which are activated and pointing toward potential etiologic agents of the associated psychosis, the methylated tertiary amines N-methyl-salsolinol, N-methyl-norsalsolinol, and adrenochrome, which appear in scientific reports concerning their association with hallucinogenic and/or neurotoxic outcomes. Electrotopological state (E-state) data has been generated for these compounds, illustrating a strong similarity with hallucinogens, particularly in terms of the E-state of the nitrogen in their tertiary amine moieties. In light of the role the folate cycle plays in transmethylation, neuroprotective strategies to prevent the transition to psychosis are suggested, including the advisory that folate supplementation can be harmful depending on the status of other relevant biochemicals. ,Christine L. Miller [PublishedText] => Published [IsEdit] => 0 [AccountId] => 78 [Zh] => 0 [AuthorsName] => Christine L. Miller ) [79] => Array ( [ArticleId] => 1310 [Create_Time] => 2024-05-27 [zipUrl] => https://www.explorationpub.com/uploads/zip/202405/20240527023742.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100480/100480.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100480/100480.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100480/100480_cover.png [JournalsId] => 7 [Title] => Advances in pharmacogenomics: optimizing antiepileptic drug therapy for drug-resistant epilepsy [Abstract] => Epilepsy, a complex neurological disorder, is influenced by intricate interactions within cortical, hippocampal, or thalamocortical neuronal networks, presenting a genetically complex condition with [AbstractComplete] =>

Epilepsy, a complex neurological disorder, is influenced by intricate interactions within cortical, hippocampal, or thalamocortical neuronal networks, presenting a genetically complex condition with non-Mendelian inheritance patterns. This complexity is underscored by the involvement of numerous “susceptibilities” or “modifier” genes, complicating the assessment of risk and therapy outcomes. A critical inquiry in epilepsy treatment involves understanding how genetic diversity impacts treatment strategies and efficacy. Pharmacogenomic advancements have elaborated the connection between genetic variants and antiseizure medication (ASM) safety and response, marking a shift towards precision medicine in epilepsy care. Notably, genetic screening for variants such as HLA-B*1502 and HLA-A*3101 has demonstrated significant efficacy in preventing severe hypersensitivity reactions, including toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS), particularly among specific ethnic populations. However, putting pharmacogenomic discoveries into clinical practice faces numerous challenges, including educational, legal, and economic barriers, emphasizing the need for broader acceptance and integration of pharmacogenomic data. This review synthesizes recent studies on pharmacogenomics in epilepsy, highlighting the current advances and prospects for personalizing epilepsy treatment through genetic insights, aiming to enhance ASM safety, reduce adverse effects, and improve treatment outcomes. Through a comprehensive examination of the genetic basis of epilepsy and its influence on pharmacotherapy, this review endeavors to contribute to the evolving landscape of precision medicine in epilepsy care, advocating for a more individualized and effective treatment approach.

[Names] => Amna Shahid ... Sameen Abbas [CName] => [Doi] => 10.37349/ent.2024.00080 [Published] => May 31, 2024 [Viewed] => 2 [Downloaded] => 0 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/ent.2024.00080 [Inline] => 0 [Type] => 0 [Issue] => 0 [Topic] => 0 [TitleAbbr] => Explor Neuroprot Ther. [Pages] => 2024;4:240–50 [Recommend] => 0 [Keywords] => Epilepsy, pharmacogenomics, antiepileptic drugs, pharmacology [DetailTitle] => [DetailUrl] => [Id] => 100480 [ris] => https://www.explorationpub.com/uploads/Article/A100480/b8c1a341b73916cfc92bc200fc16b4ec.ris [bib] => https://www.explorationpub.com/uploads/Article/A100480/b90c583efaf4852622a05ccf755fcc13.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Shahid A, Hameed K, Zainab A, Zafar A, Abbas S. Advances in pharmacogenomics: optimizing antiepileptic drug therapy for drug-resistant epilepsy. Explor Neuroprot Ther. 2024;4:240–50. https://doi.org/10.37349/ent.2024.00080 [Jindex] => 0 [CEmail] => [Ris_Time] => 2024-05-27 05:03:55 [Bib_Time] => 2024-05-27 05:03:55 [KeysWordContens] => Advances in pharmacogenomics: optimizing antiepileptic drug therapy for drug-resistant epilepsy, Epilepsy, pharmacogenomics, antiepileptic drugs, pharmacology, Epilepsy, a complex neurological disorder, is influenced by intricate interactions within cortical, hippocampal, or thalamocortical neuronal networks, presenting a genetically complex condition with non-Mendelian inheritance patterns. This complexity is underscored by the involvement of numerous “susceptibilities” or “modifier” genes, complicating the assessment of risk and therapy outcomes. A critical inquiry in epilepsy treatment involves understanding how genetic diversity impacts treatment strategies and efficacy. Pharmacogenomic advancements have elaborated the connection between genetic variants and antiseizure medication (ASM) safety and response, marking a shift towards precision medicine in epilepsy care. Notably, genetic screening for variants such as HLA-B*1502 and HLA-A*3101 has demonstrated significant efficacy in preventing severe hypersensitivity reactions, including toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS), particularly among specific ethnic populations. However, putting pharmacogenomic discoveries into clinical practice faces numerous challenges, including educational, legal, and economic barriers, emphasizing the need for broader acceptance and integration of pharmacogenomic data. This review synthesizes recent studies on pharmacogenomics in epilepsy, highlighting the current advances and prospects for personalizing epilepsy treatment through genetic insights, aiming to enhance ASM safety, reduce adverse effects, and improve treatment outcomes. Through a comprehensive examination of the genetic basis of epilepsy and its influence on pharmacotherapy, this review endeavors to contribute to the evolving landscape of precision medicine in epilepsy care, advocating for a more individualized and effective treatment approach. ,Amna Shahid ... Sameen Abbas [PublishedText] => Published [IsEdit] => 0 [AccountId] => 69 [Zh] => 0 [AuthorsName] => Amna Shahid, Kainat Hameed, Abiha Zainab, Ahsan Zafar, Sameen Abbas ) )