All living organisms exhibit circadian rhythms. Humans show circadian rhythm of the different physiological functions such as sleep-wake cycle, core body temperature, feeding behavior, metabolic activity, heart rate variability, hormone secretion, and others. The hypothalamic suprachiasmatic nucleus (SCN) acts as a primary circadian pacemaker. Peripheral tissues have an endogenous circadian clock; however, SCN synchronizes the circadian activity of the peripheral clocks. The retinohypothalamic tract (RHT) from retinal ganglionic cells carries the photic signal into the SCN that regulates the rhythmic expression of the core clock genes through the feedback loop. At the output level, the SCN connects with the pineal gland and the peripheral tissues with the help of neuroendocrine mediators. Disruption of circadian clock functions is detrimental to health. Shift work, night work, chronic or acute jet lag, and light-at-night have adverse effects on circadian functions. Misalignment of circadian rhythm alters the expression of core clock genes, leading to deregulation of cellular activity and metabolic functions. Circadian rhythm dysfunction causes many pathologic conditions, including sleep disorders, cardiovascular problems, metabolic dysfunction, infertility, poor physical performance, as well as cancer. The present work has reviewed the relationship between circadian clock dysfunction and impaired physiological activities.
[Names] => Saptadip Samanta, Sk Asif Ali [Doi] => 10.37349/en.2022.00002 [Published] => September 29, 2022 [Viewed] => 2073 [Downloaded] => 74 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2022.00002 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 82 [TitleAbbr] => Explor Neurosci. [Pages] => 2022;1:4–30 [Recommend] => 0 [Keywords] => Circadian rhythm, hypothalamic suprachiasmatic nucleus, clock genes, circadian dysfunction metabolic disorder, cancer [DetailTitle] => Circadian Rhythm and Melatonin [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/82 [Id] => 10062 [ris] => https://www.explorationpub.com/uploads/Article/A10062/9ad2e594a7d4248469e7df5f4e929ebe.ris [bib] => https://www.explorationpub.com/uploads/Article/A10062/d67e8446839d34d283ca12314b852054.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-27 [CitethisArticle] => Samanta S, Ali SA. Impact of circadian clock dysfunction on human health. Explor Neurosci. 2022;1:4-30. https://doi.org/10.37349/en.2022.00002 [Jindex] => 0 [CName] => SaptadipSamanta, [CEmail] => saptadip174@gmail.com, [Ris_Time] => 2022-09-26 08:40:52 [Bib_Time] => 2022-09-26 08:40:52 [KeysWordContens] => Impact of circadian clock dysfunction on human health, Circadian rhythm, hypothalamic suprachiasmatic nucleus, clock genes, circadian dysfunction metabolic disorder, cancer, All living organisms exhibit circadian rhythms. Humans show circadian rhythm of the different physiological functions such as sleep-wake cycle, core body temperature, feeding behavior, metabolic activity, heart rate variability, hormone secretion, and others. The hypothalamic suprachiasmatic nucleus (SCN) acts as a primary circadian pacemaker. Peripheral tissues have an endogenous circadian clock; however, SCN synchronizes the circadian activity of the peripheral clocks. The retinohypothalamic tract (RHT) from retinal ganglionic cells carries the photic signal into the SCN that regulates the rhythmic expression of the core clock genes through the feedback loop. At the output level, the SCN connects with the pineal gland and the peripheral tissues with the help of neuroendocrine mediators. Disruption of circadian clock functions is detrimental to health. Shift work, night work, chronic or acute jet lag, and light-at-night have adverse effects on circadian functions. Misalignment of circadian rhythm alters the expression of core clock genes, leading to deregulation of cellular activity and metabolic functions. Circadian rhythm dysfunction causes many pathologic conditions, including sleep disorders, cardiovascular problems, metabolic dysfunction, infertility, poor physical performance, as well as cancer. The present work has reviewed the relationship between circadian clock dysfunction and impaired physiological activities. ,Saptadip Samanta, Sk Asif Ali [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [2] => Array ( [ArticleId] => 393 [Create_Time] => 2022-09-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230520030633.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10063/10063.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10063/10063.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10063/10063_cover.png [JournalsId] => 8 [Title] => Neuregulins: subcellular localization, signaling pathways and their relationship with neuroplasticity and neurological diseases [Abstract] => Neuregulins (NRGs) and their cognate ErbB receptors (ErbB2–ErbB4) constitute a vast group of proteins encoded by six different genes (NRG1–6) and many isoforms with critical [AbstractComplete] =>Neuregulins (NRGs) and their cognate ErbB receptors (ErbB2–ErbB4) constitute a vast group of proteins encoded by six different genes (NRG1–6) and many isoforms with critical roles in the development and functioning of the nervous system. NRGs are known to regulate important processes in the nervous system like neural development, neuronal differentiation, neurite outgrowth, and specification. These factors are involved in the regulation of neurotransmission pathways and the modulation of several forms of synaptic plasticity. Due to NRGs’ role in synaptic plasticity, defects in their normal functioning are translated into altered signaling networks, which have been linked to susceptibility to developing psychiatric disorders like schizophrenia (SZ), autism, depression, and bipolar disorders. Additionally, deviation of the NRG normal functioning is involved in neurological diseases like Alzheimer’s and Parkinson’s disease. Contrastingly, NRG/ErbB signaling is also involved in the recovery after traumatic brain injuries (e.g., ischemic stroke). The NRG/ErbB signaling complex is highly unusual because the ligands (mainly NRG1–NRG3, with their multiple isoforms) and receptors (ErbB2–ErbB4) can orchestrate vast signaling complexes, with a wide reach within the processes that govern the development and appropriate function of the nervous system. This may explain why NRGs and ErbB receptor genes have been linked to complex brain disorders, like SZ. This review, are discussed important aspects of NRG and their relevance for nervous system functioning, including 1) subcellular localization, 2) signaling pathways involved in neuronal functions, 3) effect on neurite development and synapse formation, 4) modulation of some mechanisms of synaptic plasticity [long-term potentiation (LTP), depotentiation, long-term depression (LTD)] and 5) roles of NRGs in some neurological diseases. This review intends to present a summary of the main findings about this family of proteins, which might position them as one of the master regulators of brain functioning.
[Names] => Marines Longart ... Juan Carlos Martínez [Doi] => 10.37349/en.2022.00003 [Published] => September 29, 2022 [Viewed] => 1209 [Downloaded] => 41 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2022.00003 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Neurosci. [Pages] => 2022;1:31–53 [Recommend] => 0 [Keywords] => Neuregulin, ErbB receptors, synaptic plasticity, synaptogenesis [DetailTitle] => [DetailUrl] => [Id] => 10063 [ris] => https://www.explorationpub.com/uploads/Article/A10063/86148442f797822e637ee954f91d99ec.ris [bib] => https://www.explorationpub.com/uploads/Article/A10063/41e59f4f52622c3607284e28126d9e41.bib [ens] => [Cited] => 1 [Cited_Time] => 2022-11-02 [CitethisArticle] => Longart M, Calderón C, González M, Grela ME, Martínez JC. Neuregulins: subcellular localization, signaling pathways and their relationship with neuroplasticity and neurological diseases. Explor Neurosci. 2022;1:31–53. https://doi.org/10.37349/en.2022.00003 [Jindex] => 0 [CName] => MarinesLongart, [CEmail] => mlongart87@gmail.com, [Ris_Time] => 2022-09-29 01:38:53 [Bib_Time] => 2022-09-29 01:38:53 [KeysWordContens] => Neuregulins: subcellular localization, signaling pathways and their relationship with neuroplasticity and neurological diseases, Neuregulin, ErbB receptors, synaptic plasticity, synaptogenesis, Neuregulins (NRGs) and their cognate ErbB receptors (ErbB2–ErbB4) constitute a vast group of proteins encoded by six different genes (NRG1–6) and many isoforms with critical roles in the development and functioning of the nervous system. NRGs are known to regulate important processes in the nervous system like neural development, neuronal differentiation, neurite outgrowth, and specification. These factors are involved in the regulation of neurotransmission pathways and the modulation of several forms of synaptic plasticity. Due to NRGs’ role in synaptic plasticity, defects in their normal functioning are translated into altered signaling networks, which have been linked to susceptibility to developing psychiatric disorders like schizophrenia (SZ), autism, depression, and bipolar disorders. Additionally, deviation of the NRG normal functioning is involved in neurological diseases like Alzheimer’s and Parkinson’s disease. Contrastingly, NRG/ErbB signaling is also involved in the recovery after traumatic brain injuries (e.g., ischemic stroke). The NRG/ErbB signaling complex is highly unusual because the ligands (mainly NRG1–NRG3, with their multiple isoforms) and receptors (ErbB2–ErbB4) can orchestrate vast signaling complexes, with a wide reach within the processes that govern the development and appropriate function of the nervous system. This may explain why NRGs and ErbB receptor genes have been linked to complex brain disorders, like SZ. This review, are discussed important aspects of NRG and their relevance for nervous system functioning, including 1) subcellular localization, 2) signaling pathways involved in neuronal functions, 3) effect on neurite development and synapse formation, 4) modulation of some mechanisms of synaptic plasticity [long-term potentiation (LTP), depotentiation, long-term depression (LTD)] and 5) roles of NRGs in some neurological diseases. This review intends to present a summary of the main findings about this family of proteins, which might position them as one of the master regulators of brain functioning. ,Marines Longart ... Juan Carlos Martínez [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [3] => Array ( [ArticleId] => 394 [Create_Time] => 2022-09-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202210/20221021062432.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10064/10064.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10064/10064.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10064/10061_Cover.png [JournalsId] => 8 [Title] => Recent developments and future perspectives of neuropathology [Abstract] => This brief statement describes some recent achievements of neuropathological research, with the focus on Alzheimer’s and other age-related diseases, neurodegenerative disorders (tauopathies, synucleinopathies), multimorbidity of the aged brain, multiple sclerosis (MS), and other neuroinflammatory disorders, including central nervous system involvement by coronavirus disease 2019 (COVID-19), as well as new developments in neurovascular diseases, neurooncology, and myopathies. Although neuropathology, using modern technologies, such as cryo-electron microscopy, proteomic and experimental methods, has helped to increase diagnostic accuracy and provided insight into the pathogenesis of many neurological disorders, future studies in co-operation with clinical and other neurosciences should overcome the challenges of disease-influencing therapeutic approaches. [AbstractComplete] =>This brief statement describes some recent achievements of neuropathological research, with the focus on Alzheimer’s and other age-related diseases, neurodegenerative disorders (tauopathies, synucleinopathies), multimorbidity of the aged brain, multiple sclerosis (MS), and other neuroinflammatory disorders, including central nervous system involvement by coronavirus disease 2019 (COVID-19), as well as new developments in neurovascular diseases, neurooncology, and myopathies. Although neuropathology, using modern technologies, such as cryo-electron microscopy, proteomic and experimental methods, has helped to increase diagnostic accuracy and provided insight into the pathogenesis of many neurological disorders, future studies in co-operation with clinical and other neurosciences should overcome the challenges of disease-influencing therapeutic approaches.
[Names] => Kurt A. Jellinger [Doi] => 10.37349/en.2022.00004 [Published] => September 30, 2022 [Viewed] => 1826 [Downloaded] => 49 [Subject] => Perspective [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2022.00004 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Neurosci. [Pages] => 2022;1:54–60 [Recommend] => 1 [Keywords] => Neuropathology, neurodegenerative diseases, Alzheimer’s disease, movement disorders, neurooncology, neuroinflammation [DetailTitle] => [DetailUrl] => [Id] => 10064 [ris] => https://www.explorationpub.com/uploads/Article/A10064/5abdd6f250f042d7b9770118979fb055.ris [bib] => https://www.explorationpub.com/uploads/Article/A10064/baa83497a8d8beaee113d7d6d77f590f.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-27 [CitethisArticle] => Jellinger KA. Recent developments and future perspectives of neuropathology. Explor Neurosci. 2022;1:54–60. https://doi.org/10.37349/en.2022.00004 [Jindex] => 0 [CName] => Kurt A.Jellinger, [CEmail] => kurt.jellinger@univie.ac.at, [Ris_Time] => 2022-09-29 01:55:53 [Bib_Time] => 2022-09-29 01:55:53 [KeysWordContens] => Recent developments and future perspectives of neuropathology, Neuropathology, neurodegenerative diseases, Alzheimer’s disease, movement disorders, neurooncology, neuroinflammation, This brief statement describes some recent achievements of neuropathological research, with the focus on Alzheimer’s and other age-related diseases, neurodegenerative disorders (tauopathies, synucleinopathies), multimorbidity of the aged brain, multiple sclerosis (MS), and other neuroinflammatory disorders, including central nervous system involvement by coronavirus disease 2019 (COVID-19), as well as new developments in neurovascular diseases, neurooncology, and myopathies. Although neuropathology, using modern technologies, such as cryo-electron microscopy, proteomic and experimental methods, has helped to increase diagnostic accuracy and provided insight into the pathogenesis of many neurological disorders, future studies in co-operation with clinical and other neurosciences should overcome the challenges of disease-influencing therapeutic approaches. ,Kurt A. Jellinger [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [4] => Array ( [ArticleId] => 397 [Create_Time] => 2022-10-09 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230523062304.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10065/10065.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10065/10065.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10065/10065_cover.png [JournalsId] => 8 [Title] => Neuroprotective and neurorestorative actions of mesenchymal stromal cell-derived small extracellular vesicles in the ischemic brain [Abstract] => Ischemic stroke is a highly prevalent condition that frequently results in life-long disability and death. Considerable efforts have been made to establish treatments that prevent secondary ischemic [AbstractComplete] =>Ischemic stroke is a highly prevalent condition that frequently results in life-long disability and death. Considerable efforts have been made to establish treatments that prevent secondary ischemic damage and promote stroke recovery. Until now, the recanalization of occluded blood vessels via thrombolysis and thrombectomy, although highly potent, remains the only treatment in humans that enhances stroke outcome. Small extracellular vesicles are non-replicating, nano-sized (70–150 nm) lipid bilayer-enclosed vesicles, which have shown remarkable biological activities in various physiological and pathophysiological contexts. When administered post-stroke, mesenchymal stromal cell-derived extracellular vesicles (MSC-EVs) induce neuroprotection, promote brain remodeling and plasticity, and enhance neurological recovery in rodents and non-human primates via mechanisms that involve immunomodulation and anti-inflammation. In this review, experimental studies on the therapeutic actions of MSC-EVs in animal stroke models are summarized and perspectives for clinical translation are outlined.
[Names] => Chen Wang ... Dirk M. Hermann [Doi] => 10.37349/en.2022.00005 [Published] => October 09, 2022 [Viewed] => 1659 [Downloaded] => 48 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2022.00005 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 76 [TitleAbbr] => Explor Neurosci. [Pages] => 2022;1:61–74 [Recommend] => 0 [Keywords] => Ischemic stroke, exosome, microparticle, anti-inflammation, immunomodulation, leukocyte, microglia, polymorphonuclear neutrophil [DetailTitle] => Extracellular Vesicles as Cell-based Therapeutics [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/76 [Id] => 10065 [ris] => https://www.explorationpub.com/uploads/Article/A10065/10e6e1a706f948b777ae652aa4c5e1d6.ris [bib] => https://www.explorationpub.com/uploads/Article/A10065/804fac5bf84a992519ab8c6c1587bfcd.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Wang C, Giebel B, Hermann DM. Neuroprotective and neurorestorative actions of mesenchymal stromal cell-derived small extracellular vesicles in the ischemic brain. Explor Neurosci. 2022;1:61–74. https://doi.org/10.37349/en.2022.00005 [Jindex] => 0 [CName] => Dirk M.Hermann, [CEmail] => dirk.hermann@uk-essen.de, [Ris_Time] => 2022-10-09 02:31:57 [Bib_Time] => 2022-10-09 02:31:57 [KeysWordContens] => Neuroprotective and neurorestorative actions of mesenchymal stromal cell-derived small extracellular vesicles in the ischemic brain, Ischemic stroke, exosome, microparticle, anti-inflammation, immunomodulation, leukocyte, microglia, polymorphonuclear neutrophil, Ischemic stroke is a highly prevalent condition that frequently results in life-long disability and death. Considerable efforts have been made to establish treatments that prevent secondary ischemic damage and promote stroke recovery. Until now, the recanalization of occluded blood vessels via thrombolysis and thrombectomy, although highly potent, remains the only treatment in humans that enhances stroke outcome. Small extracellular vesicles are non-replicating, nano-sized (70–150 nm) lipid bilayer-enclosed vesicles, which have shown remarkable biological activities in various physiological and pathophysiological contexts. When administered post-stroke, mesenchymal stromal cell-derived extracellular vesicles (MSC-EVs) induce neuroprotection, promote brain remodeling and plasticity, and enhance neurological recovery in rodents and non-human primates via mechanisms that involve immunomodulation and anti-inflammation. In this review, experimental studies on the therapeutic actions of MSC-EVs in animal stroke models are summarized and perspectives for clinical translation are outlined. ,Chen Wang ... Dirk M. Hermann [PublishedText] => Published [IsEdit] => 0 [AccountId] => 0 [Zh] => 1 ) [5] => Array ( [ArticleId] => 439 [Create_Time] => 2022-12-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230523063312.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10066/10066.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10066/10066.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10066/10066_cover.png [JournalsId] => 8 [Title] => Should we rethink neurodegeneration? [Abstract] => The therapy of many neurological disorders has advanced markedly during recent decades. Not so for neurodegenerative disorders. Early detection, deep individual genotyping and phenotyping, and perso [AbstractComplete] =>The therapy of many neurological disorders has advanced markedly during recent decades. Not so for neurodegenerative disorders. Early detection, deep individual genotyping and phenotyping, and personalized therapies have been suggested as the way forward. However, we still do not know enough about the aetiology and molecular basics of these diseases. In fact, the term neurodegenerative disorder may be a misleading categorization that constitutes a major cognitive barrier against better characterization and understanding of these disorders. Therefore, we need to go back to the basics and employ novel, open-minded observational study protocols that combine very extensive and robust clinical, molecular and epidemiological data collection methods. Moreover, we need to reconsider our basic orientation towards these diseases to increase our chances of finding out what we are actually trying to care for and cure.
[Names] => Jussi O. T. Sipilä [Doi] => 10.37349/en.2022.00006 [Published] => December 26, 2022 [Viewed] => 676 [Downloaded] => 22 [Subject] => Perspective [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2022.00006 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neurosci. [Pages] => 2022;1:75–82 [Recommend] => 0 [Keywords] => Biomarkers, diagnosis, neurodegeneration, neuroepidemiology, neuropathology, treatment trials [DetailTitle] => [DetailUrl] => [Id] => 10066 [ris] => https://www.explorationpub.com/uploads/Article/A10066/9fe23ec38e27dc66df57afa450e228e9.ris [bib] => https://www.explorationpub.com/uploads/Article/A10066/3a910faeefc708de000f9eb141ac8aba.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Sipilä JOT. Should we rethink neurodegeneration? Explor Neurosci. 2022;1:75–82. https://doi.org/10.37349/en.2022.00006 [Jindex] => 0 [CName] => Jussi O. T.Sipilä, [CEmail] => jussi.sipila@utu.fi, [Ris_Time] => 2022-12-26 07:19:49 [Bib_Time] => 2022-12-26 07:19:49 [KeysWordContens] => Should we rethink neurodegeneration?, Biomarkers, diagnosis, neurodegeneration, neuroepidemiology, neuropathology, treatment trials, The therapy of many neurological disorders has advanced markedly during recent decades. Not so for neurodegenerative disorders. Early detection, deep individual genotyping and phenotyping, and personalized therapies have been suggested as the way forward. However, we still do not know enough about the aetiology and molecular basics of these diseases. In fact, the term neurodegenerative disorder may be a misleading categorization that constitutes a major cognitive barrier against better characterization and understanding of these disorders. Therefore, we need to go back to the basics and employ novel, open-minded observational study protocols that combine very extensive and robust clinical, molecular and epidemiological data collection methods. Moreover, we need to reconsider our basic orientation towards these diseases to increase our chances of finding out what we are actually trying to care for and cure. ,Jussi O. T. Sipilä [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [6] => Array ( [ArticleId] => 459 [Create_Time] => 2022-12-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230523070126.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10067/10067.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10067/10067.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10067/10067_cover.png [JournalsId] => 8 [Title] => Updates in mechanical thrombectomy [Abstract] => Stroke is a leading cause of morbidity and mortality. The advent of mechanical thrombectomy has largely improved patient outcomes. This article reviews the features and outcomes associated with aspi [AbstractComplete] =>Stroke is a leading cause of morbidity and mortality. The advent of mechanical thrombectomy has largely improved patient outcomes. This article reviews the features and outcomes associated with aspiration, stent retrievers, and combination catheters used in current practice. There is also a discussion on clinical considerations based on anatomical features and clot composition. The reperfusion grading scale and outcome metrics commonly used following thrombectomy when a patient is still in the hospital are reviewed. Lastly, there are proposed discharge and outpatient follow-up goals in caring for patients hospitalized for a stroke.
[Names] => Kevin Pierre ... Brandon Lucke-Wold [Doi] => 10.37349/en.2022.00007 [Published] => December 30, 2022 [Viewed] => 2018 [Downloaded] => 54 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2022.00007 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 115 [TitleAbbr] => Explor Neurosci. [Pages] => 2022;1:83–99 [Recommend] => 1 [Keywords] => Stroke, ischemic infarct, mechanical thrombectomy, catheters, aspiration, stent retrievers [DetailTitle] => Emerging Trends in Endovascular Management [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/115 [Id] => 10067 [ris] => https://www.explorationpub.com/uploads/Article/A10067/558b794181280f7b890446634f5d6f2f.ris [bib] => https://www.explorationpub.com/uploads/Article/A10067/d71832469333d828f45d66047495a356.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-04-27 [CitethisArticle] => Pierre K, Perez-Vega C, Fusco A, Olowofela B, Hatem R, Elyazeed M, et al. Updates in mechanical thrombectomy. Explor Neurosci. 2022;1:83–99. https://doi.org/10.37349/en.2022.00007 [Jindex] => 0 [CName] => KevinPierre, [CEmail] => kpierre150@gmail.com, [Ris_Time] => 2022-12-28 07:36:46 [Bib_Time] => 2022-12-30 01:37:24 [KeysWordContens] => Updates in mechanical thrombectomy, Stroke, ischemic infarct, mechanical thrombectomy, catheters, aspiration, stent retrievers, Stroke is a leading cause of morbidity and mortality. The advent of mechanical thrombectomy has largely improved patient outcomes. This article reviews the features and outcomes associated with aspiration, stent retrievers, and combination catheters used in current practice. There is also a discussion on clinical considerations based on anatomical features and clot composition. The reperfusion grading scale and outcome metrics commonly used following thrombectomy when a patient is still in the hospital are reviewed. Lastly, there are proposed discharge and outpatient follow-up goals in caring for patients hospitalized for a stroke. ,Kevin Pierre ... Brandon Lucke-Wold [PublishedText] => Published [IsEdit] => 0 [AccountId] => 46 [Zh] => 1 ) [7] => Array ( [ArticleId] => 461 [Create_Time] => 2022-12-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230524070537.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10068/10068.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10068/10068.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10068/10068_cover.png [JournalsId] => 8 [Title] => Cellular and molecular mechanisms of stress-induced memory impairment [Abstract] => Exposure to stressful conditions plays a critical role in brain processes, including neural plasticity, synaptic transmission, and cognitive functions. Since memory-related brain regions, the hippocampus (Hip), the amygdala, and the prefrontal cortex, express high glucocorticoid receptors (GRs), these areas are the potential targets of stress hormones. Stress affects memory encoding, consolidation, and retrieval, which may depend on many factors such as the type, duration, the intensity of the stressor or the brain region. Here, this review mainly focused on the mechanisms involved in stress-induced memory impairment. Acute/chronic stress induces structural and functional changes in neurons and glial cells. Dendritic arborization, reduction of dendritic spine density, and alteration in glutamatergic-mediated synaptic transmission via N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors are mechanisms that stress affect long-term memory formation. Exposure to acute or chronic stress could interplay with multiple neurotransmitter signaling, modulating the neuronal circuits involved in memory impairment or state-dependent learning. Stress hormones also modulate the expression of microRNAs in the specific brain regions responsible for stress-induced behaviors. Because of expressing GRs in astrocytes and microglial cells, stress could affect the morphology, structure, and functions of these glial cells in memory-related brain regions. Astrocytes play a crucial role in stress-induced aversive or fear memory formation. Over-activation of the microglial cells enhances the release of inflammatory cytokines, which results in neuronal injury. Stress has a prominent role in cognitive decline to induces memory problems, particularly in older adults. Due to the issue’s importance, here the provided overview attempted to address the question of how stress alters neuronal epigenetic regulators, synaptic transmissions, and glial activity in the brain. [AbstractComplete] =>Exposure to stressful conditions plays a critical role in brain processes, including neural plasticity, synaptic transmission, and cognitive functions. Since memory-related brain regions, the hippocampus (Hip), the amygdala, and the prefrontal cortex, express high glucocorticoid receptors (GRs), these areas are the potential targets of stress hormones. Stress affects memory encoding, consolidation, and retrieval, which may depend on many factors such as the type, duration, the intensity of the stressor or the brain region. Here, this review mainly focused on the mechanisms involved in stress-induced memory impairment. Acute/chronic stress induces structural and functional changes in neurons and glial cells. Dendritic arborization, reduction of dendritic spine density, and alteration in glutamatergic-mediated synaptic transmission via N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors are mechanisms that stress affect long-term memory formation. Exposure to acute or chronic stress could interplay with multiple neurotransmitter signaling, modulating the neuronal circuits involved in memory impairment or state-dependent learning. Stress hormones also modulate the expression of microRNAs in the specific brain regions responsible for stress-induced behaviors. Because of expressing GRs in astrocytes and microglial cells, stress could affect the morphology, structure, and functions of these glial cells in memory-related brain regions. Astrocytes play a crucial role in stress-induced aversive or fear memory formation. Over-activation of the microglial cells enhances the release of inflammatory cytokines, which results in neuronal injury. Stress has a prominent role in cognitive decline to induces memory problems, particularly in older adults. Due to the issue’s importance, here the provided overview attempted to address the question of how stress alters neuronal epigenetic regulators, synaptic transmissions, and glial activity in the brain.
[Names] => Ameneh Rezayof ... Shiva Hashemizadeh [Doi] => 10.37349/en.2022.00008 [Published] => December 30, 2022 [Viewed] => 935 [Downloaded] => 48 [Subject] => Review [Year] => 2022 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2022.00008 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 78 [TitleAbbr] => Explor Neurosci. [Pages] => 2022;1:100–119 [Recommend] => 0 [Keywords] => Stress, memory impairment, neurotransmitters, astrocytes, microglia, microRNAs [DetailTitle] => Neuroinflammation in the Ageing and the Injured Brain [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/78 [Id] => 10068 [ris] => https://www.explorationpub.com/uploads/Article/A10068/2217d33157c83a509b36becf3e44f8e4.ris [bib] => https://www.explorationpub.com/uploads/Article/A10068/8d74cfaf664f465dcdca178a7ebc6562.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Rezayof A, Sardari M, Hashemizadeh S. Cellular and molecular mechanisms of stress-induced memory impairment. Explor Neurosci. 2022;1:100-19. https://doi.org/10.37349/en.2022.00008 [Jindex] => 0 [CName] => AmenehRezayof, [CEmail] => arezayof@ut.a.c.ir, [Ris_Time] => 2022-12-28 07:53:25 [Bib_Time] => 2022-12-28 07:53:25 [KeysWordContens] => Cellular and molecular mechanisms of stress-induced memory impairment, Stress, memory impairment, neurotransmitters, astrocytes, microglia, microRNAs, Exposure to stressful conditions plays a critical role in brain processes, including neural plasticity, synaptic transmission, and cognitive functions. Since memory-related brain regions, the hippocampus (Hip), the amygdala, and the prefrontal cortex, express high glucocorticoid receptors (GRs), these areas are the potential targets of stress hormones. Stress affects memory encoding, consolidation, and retrieval, which may depend on many factors such as the type, duration, the intensity of the stressor or the brain region. Here, this review mainly focused on the mechanisms involved in stress-induced memory impairment. Acute/chronic stress induces structural and functional changes in neurons and glial cells. Dendritic arborization, reduction of dendritic spine density, and alteration in glutamatergic-mediated synaptic transmission via N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors are mechanisms that stress affect long-term memory formation. Exposure to acute or chronic stress could interplay with multiple neurotransmitter signaling, modulating the neuronal circuits involved in memory impairment or state-dependent learning. Stress hormones also modulate the expression of microRNAs in the specific brain regions responsible for stress-induced behaviors. Because of expressing GRs in astrocytes and microglial cells, stress could affect the morphology, structure, and functions of these glial cells in memory-related brain regions. Astrocytes play a crucial role in stress-induced aversive or fear memory formation. Over-activation of the microglial cells enhances the release of inflammatory cytokines, which results in neuronal injury. Stress has a prominent role in cognitive decline to induces memory problems, particularly in older adults. Due to the issue’s importance, here the provided overview attempted to address the question of how stress alters neuronal epigenetic regulators, synaptic transmissions, and glial activity in the brain. ,Ameneh Rezayof ... Shiva Hashemizadeh [PublishedText] => Published [IsEdit] => 0 [AccountId] => 47 [Zh] => 1 ) [8] => Array ( [ArticleId] => 479 [Create_Time] => 2023-02-23 [zipUrl] => https://www.explorationpub.com/uploads/zip/202305/20230525034311.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A10069/10069.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A10069/10069.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A10069/10069_Cover.png [JournalsId] => 8 [Title] => Update for astrocytomas: medical and surgical management considerations [Abstract] => Astrocytomas include a wide range of tumors with unique mutations and varying grades of malignancy. These tumors all originate from the astrocyte, a star-shaped glial cell that plays a major role in [AbstractComplete] =>Astrocytomas include a wide range of tumors with unique mutations and varying grades of malignancy. These tumors all originate from the astrocyte, a star-shaped glial cell that plays a major role in supporting functions of the central nervous system (CNS), including blood-brain barrier (BBB) development and maintenance, water and ion regulation, influencing neuronal synaptogenesis, and stimulating the immunological response. In terms of epidemiology, glioblastoma (GB), the most common and malignant astrocytoma, generally occur with higher rates in Australia, Western Europe, and Canada, with the lowest rates in Southeast Asia. Additionally, significantly higher rates of GB are observed in males and non-Hispanic whites. It has been suggested that higher levels of testosterone observed in biological males may account for the increased rates of GB. Hereditary syndromes such as Cowden, Lynch, Turcot, Li-Fraumeni, and neurofibromatosis type 1 have been linked to increased rates of astrocytoma development. While there are a number of specific gene mutations that may influence malignancy or be targeted in astrocytoma treatment, O6-methylguanine-DNA methyltransferase (MGMT) gene function is an important predictor of astrocytoma response to chemotherapeutic agent temozolomide (TMZ). TMZ for primary and bevacizumab in the setting of recurrent tumor formation are two of the main chemotherapeutic agents currently approved in the treatment of astrocytomas. While stereotactic radiosurgery (SRS) has debatable implications for increased survival in comparison to whole-brain radiotherapy (WBRT), SRS demonstrates increased precision with reduced radiation toxicity. When considering surgical resection of astrocytoma, the extent of resection (EoR) is taken into consideration. Subtotal resection (STR) spares the margins of the T1 enhanced magnetic resonance imaging (MRI) region, gross total resection (GTR) includes the margins, and supramaximal resection (SMR) extends beyond the margin of the T1 and into the T2 region. Surgical resection, radiation, and chemotherapy are integral components of astrocytoma treatment.
Hereditary risk factors, genetic mutations, and imaging modalities are discussed in reference to astrocytoma staging and mechanism of growth. In terms of the treatment of astrocytomas, chemotherapy, radiation therapy, and strategic surgical interventions are discussed
Stroke is one of the leading causes of death and disability worldwide. Plasma biomarkers have long been used to evaluate physiological or pathological processes and to make predictions about the outcome of stroke patients. The current systematic review is focused on genetic plasma biomarkers as a new potential prognostic indicator for post-stroke recovery. The aim of the present systematic review is to assess the potential of genetic plasma biomarkers associated with stroke to predict post-stroke recovery.
The search strategy used PubMed and Web of Science databases to identified 166 studies that investigated genetic plasma biomarkers in patients with stroke between 2017 and 2021. However, only 21 of them met the inclusion criteria.
The identified genetic biomarkers can be divided into: (i) serum/plasma circular RNA (circRNA) associated with stroke onset or recurrence (5; 23.80%), (ii) genetic polymorphisms associated with the atherosclerotic process and stroke recurrence (6; 28.57%), (iii) serum/plasma long non-coding RNA (lncRNA) levels involved in immunity/inflammatory processes (4; 19.04%), (iv) marker of DNA methylation associated with stroke onset and outcome (3; 14.28%), and (v) proteins and pathways of stroke identified by serum/ plasma proteomics/genomics analysis (3; 14.28%).
Overall, more than 100 potential biomarkers were found and the data suggest that combinations of plasma genetic biomarkers might be used as a better predictor for stroke.
Microglial activation is increasingly recognised as a factor in the progression of Alzheimer’s disease (AD) and may be modified by systemic inflammatory signals including serum tumour necrosis factor (TNF)-α. The aim was to investigate whether blockade of peripheral TNF-α with peripheral inhibitors such as etanercept reduces microglial activation in prodromal AD.
A one-year, multi-centre, phase 2, double-blind randomised placebo-controlled trial (RPCT) was performed, to assess the effect of weekly 50 mg s.c. etanercept in amyloid positive mild cognitive impaired participants on the change in microglial activation as measured by [11C](R)-PK11195 positron emission tomography (PET). Secondary objectives were to ascertain the change in cortical amyloid load on PET and the change in the Montreal Cognitive Assessment (MoCA).
Forty-four subjects consented to the study. Twenty-eight subjects failed screening including six subjects who were amyloid negative on visual read of the AmyvidTM PET scans. Thirteen of sixteen subjects with mild cognitive impairment (MCI) due to AD completed the baseline [11C](R)-PK11195 PET scan and were randomised to either placebo or etanercept. Three patients who consented were not able to complete screening due to early termination of the study following delays in study commencement. [11C](R)-PK11195 binding potential (BP) at baseline showed an almost global increase in MCI patients as compared to age-matched controls. Compliance to medication was high over the twelve-month trial period with etanercept being well tolerated. The study did not achieve statistical power to show a significant effect of etanercept over 52 weeks in the limited number of patients with MCI on microglial activation as measured by [11C](R)-PK11195 PET. Overall uptake of florbetapir in the follow up (FU) scans remained stable. The study was not powered to show statistical differences in psychometric ratings between groups.
This study did not show evidence that treatment with etanercept over one year would modulate microglial activation in amyloid positive MCI patients (EudraCT identifier: 2015-002145-63, https://www.clinicaltrialsregister.eu; International Standard Randomised Controlled Trial Number identifier: ISRCTN12472821, https://www.isrctn.com).
Despite decades of intensive research, effective treatment and prevention strategies for neurodegenerative diseases (NDDs) remain elusive. This review focuses on Alzheimer’s and Parkinson’s diseases and acquired epilepsy suggesting that in their early phase, these progressive pathologies share common or interacting molecular pathways. Indeed, oxidative stress associated with disrupted glucose metabolism is the expected end state of most, if not all, risk factors preceding the onset of major NDDs. This review proposes that the initial oxidative stress in the brain resulting specifically from the hyperactivation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) causes a decline in glucose utilization and is the primary initiating factor of major NDDs. The existing clinical and experimental evidence points to NOX as the primary initiating mechanism shared within the major NDDs. During early oxidative stress, NOX activation is triggered in variable brain cells via multiple pathways, from beta-amyloid to alpha-synuclein, fibrin to glutamate and seizures. Therefore, the treatment strategy should have targeted the activation of NOX, wouldn’t there be a lack of clinically approved selective NOX antagonists? On the other hand, there are promising metabolism-altering approaches via dietary means able to switch energy intake from glucose to ketones, which influences both oxidative stress and glucose utilization and could ameliorate disease progression. The regimen of time-restricted eating appears to be the most feasible, nutritious, and palatable one providing the essential benefits of a ketogenic diet without adverse effects.
[Names] => Yuri Zilberter, Tanya Zilberter [Doi] => 10.37349/en.2023.00013 [Published] => April 21, 2023 [Viewed] => 1607 [Downloaded] => 43 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00013 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:67–81 [Recommend] => 1 [Keywords] => Glucose metabolism, ketogenic diet, Alzheimer’s disease, beta-amyloid, Parkinson’s disease, oxidative stress, nicotinamide adenine dinucleotide phosphate oxidase, acquired epilepsy [DetailTitle] => [DetailUrl] => [Id] => 100613 [ris] => https://www.explorationpub.com/uploads/Article/A100613/e87e7e95c2a8868e3a1e8f72a6f7c1b4.ris [bib] => https://www.explorationpub.com/uploads/Article/A100613/47f6ad3f9f35325b25930da76505532f.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Zilberter Y, Zilberter T. Metabolic correction of neurodegenerative pathologies: the role of macronutrients and timing. Explor Neurosci. 2023;2:67–81. https://doi.org/10.37349/en.2023.00013 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-04-19 05:17:46 [Bib_Time] => 2023-04-19 05:17:46 [KeysWordContens] => Metabolic correction of neurodegenerative pathologies: the role of macronutrients and timing, Glucose metabolism, ketogenic diet, Alzheimer’s disease, beta-amyloid, Parkinson’s disease, oxidative stress, nicotinamide adenine dinucleotide phosphate oxidase, acquired epilepsy, Despite decades of intensive research, effective treatment and prevention strategies for neurodegenerative diseases (NDDs) remain elusive. This review focuses on Alzheimer’s and Parkinson’s diseases and acquired epilepsy suggesting that in their early phase, these progressive pathologies share common or interacting molecular pathways. Indeed, oxidative stress associated with disrupted glucose metabolism is the expected end state of most, if not all, risk factors preceding the onset of major NDDs. This review proposes that the initial oxidative stress in the brain resulting specifically from the hyperactivation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) causes a decline in glucose utilization and is the primary initiating factor of major NDDs. The existing clinical and experimental evidence points to NOX as the primary initiating mechanism shared within the major NDDs. During early oxidative stress, NOX activation is triggered in variable brain cells via multiple pathways, from beta-amyloid to alpha-synuclein, fibrin to glutamate and seizures. Therefore, the treatment strategy should have targeted the activation of NOX, wouldn’t there be a lack of clinically approved selective NOX antagonists? On the other hand, there are promising metabolism-altering approaches via dietary means able to switch energy intake from glucose to ketones, which influences both oxidative stress and glucose utilization and could ameliorate disease progression. The regimen of time-restricted eating appears to be the most feasible, nutritious, and palatable one providing the essential benefits of a ketogenic diet without adverse effects. ,Yuri Zilberter, Tanya Zilberter [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [13] => Array ( [ArticleId] => 548 [Create_Time] => 2023-04-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202304/20230425004748.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100614/100614.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100614/100614.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100614/100614_cover.png [JournalsId] => 8 [Title] => Inflammatory responses involved in post-cardiac arrest brain injury: mechanisms, regulation, and therapeutic potential [Abstract] => Neuroinflammation plays a key role in the pathogenesis of post-cardiac arrest (CA) brain injury. Innate immune cells sense a variety of danger signals through pattern-recognition receptors and evoke [AbstractComplete] =>Neuroinflammation plays a key role in the pathogenesis of post-cardiac arrest (CA) brain injury. Innate immune cells sense a variety of danger signals through pattern-recognition receptors and evoke rapidly after ischemic challenge, triggering inflammatory responses and amplifying brain damage. A programmed cell death (PCD) pathway is activated after ischemic and/or inflammatory stimuli, leading to the elimination of the damaged cells. However, PCD also regulates inflammatory responses flexibly. The present review aimed to summarize the mechanisms of inflammatory responses, including the biology of immune cells, the innate immune recognition that initiates the inflammation, and the immunomodulatory effects of PCD following CA. Promising therapeutic approaches of targeting inflammatory responses to alleviate brain injury and improve neurological outcomes after CA are also reviewed.
[Names] => Yuzhen Zhang ... Kaibin Huang [Doi] => 10.37349/en.2023.00014 [Published] => April 26, 2023 [Viewed] => 1036 [Downloaded] => 50 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00014 [Inline] => 1 [Type] => 1 [Issue] => 2 [Topic] => 0 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:82–97 [Recommend] => 0 [Keywords] => Cardiac arrest, neuroinflammation, innate immune recognition, programmed cell death, microglia [DetailTitle] => [DetailUrl] => [Id] => 100614 [ris] => https://www.explorationpub.com/uploads/Article/A100614/499a00d9214436537c402aee9c7f8371.ris [bib] => https://www.explorationpub.com/uploads/Article/A100614/6de3db712c7ca5232b9deefc5bff814e.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Zhang Y, Li Z, Zhang K, Chang Y, Chen J, Al-Nusaif M, et al. Inflammatory responses involved in post-cardiac arrest brain injury: mechanisms, regulation, and therapeutic potential. Explor Neurosci. 2023;2:82–97. https://doi.org/10.37349/en.2023.00014 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-04-23 02:00:59 [Bib_Time] => 2023-04-23 02:00:59 [KeysWordContens] => Inflammatory responses involved in post-cardiac arrest brain injury: mechanisms, regulation, and therapeutic potential, Cardiac arrest, neuroinflammation, innate immune recognition, programmed cell death, microglia, Neuroinflammation plays a key role in the pathogenesis of post-cardiac arrest (CA) brain injury. Innate immune cells sense a variety of danger signals through pattern-recognition receptors and evoke rapidly after ischemic challenge, triggering inflammatory responses and amplifying brain damage. A programmed cell death (PCD) pathway is activated after ischemic and/or inflammatory stimuli, leading to the elimination of the damaged cells. However, PCD also regulates inflammatory responses flexibly. The present review aimed to summarize the mechanisms of inflammatory responses, including the biology of immune cells, the innate immune recognition that initiates the inflammation, and the immunomodulatory effects of PCD following CA. Promising therapeutic approaches of targeting inflammatory responses to alleviate brain injury and improve neurological outcomes after CA are also reviewed. ,Yuzhen Zhang ... Kaibin Huang [PublishedText] => Published [IsEdit] => 0 [AccountId] => 57 [Zh] => 1 ) [14] => Array ( [ArticleId] => 620 [Create_Time] => 2023-06-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230628095131.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100615/100615.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100615/100615.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100615/100615_Cover.png [JournalsId] => 8 [Title] => Mesenchymal stem cell stroke therapy: current limitations in its clinical translation [Abstract] => For more than a decade now, research studies, proof of concept work, and clinical trials have endeavored to understand how mesenchymal stem cells might be used to help protect, repair, and/or regene [AbstractComplete] =>For more than a decade now, research studies, proof of concept work, and clinical trials have endeavored to understand how mesenchymal stem cells might be used to help protect, repair, and/or regenerate damaged brain tissue following stroke. To date, the majority of studies have not demonstrated significant improvements in either morbidity or medium-long-term outcome, although safety has been relatively well proven. Limitations are likely to be linked to the pathobiological complexity and seriousness of stroke tissue damage, low efficacy of treatment, and short half-life of bio-active proteins released by stem cells. This article will highlight the heterogeneity and limitation of completed studies and the current status of ongoing work. At the same time, the potential of other combinational type treatments, such as drug-loading and targeting, and the use of hydrogels is discussed.
[Names] => Ylenia Pastorello, Mark Slevin [Doi] => 10.37349/en.2023.00015 [Published] => June 28, 2023 [Viewed] => 786 [Downloaded] => 29 [Subject] => Perspective [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00015 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 78 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:98–105 [Recommend] => 0 [Keywords] => Mesenchymal stem cells, stroke, drug-loading, drug targeting [DetailTitle] => Neuroinflammation in the Ageing and the Injured Brain [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/78 [Id] => 100615 [ris] => https://www.explorationpub.com/uploads/Article/A100615/c6fa9634ecfca65c1774f4e32fadb4c5.ris [bib] => https://www.explorationpub.com/uploads/Article/A100615/230bce33ba75463a16e41c8d33dd1f44.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Pastorello Y, Slevin M. Mesenchymal stem cell stroke therapy: current limitations in its clinical translation. Explor Neurosci. 2023;2:98–105. https://doi.org/10.37349/en.2023.00015 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-06-27 08:32:30 [Bib_Time] => 2023-06-27 08:32:30 [KeysWordContens] => Mesenchymal stem cell stroke therapy: current limitations in its clinical translation, Mesenchymal stem cells, stroke, drug-loading, drug targeting, For more than a decade now, research studies, proof of concept work, and clinical trials have endeavored to understand how mesenchymal stem cells might be used to help protect, repair, and/or regenerate damaged brain tissue following stroke. To date, the majority of studies have not demonstrated significant improvements in either morbidity or medium-long-term outcome, although safety has been relatively well proven. Limitations are likely to be linked to the pathobiological complexity and seriousness of stroke tissue damage, low efficacy of treatment, and short half-life of bio-active proteins released by stem cells. This article will highlight the heterogeneity and limitation of completed studies and the current status of ongoing work. At the same time, the potential of other combinational type treatments, such as drug-loading and targeting, and the use of hydrogels is discussed. ,Ylenia Pastorello, Mark Slevin [PublishedText] => Published [IsEdit] => 0 [AccountId] => 38 [Zh] => 1 ) [15] => Array ( [ArticleId] => 630 [Create_Time] => 2023-06-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202306/20230630010200.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100616/100616.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100616/100616.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100616/100616_cover.png [JournalsId] => 8 [Title] => Therapeutic potential of extracellular vesicles in Parkinson’s disease [Abstract] => Globally, the incidence of Parkinson’s disease (PD) is increasing faster than other neurodegenerative disorders. Neuropathologically, PD is characterized by the loss of dopaminergic neurons in the [AbstractComplete] =>Globally, the incidence of Parkinson’s disease (PD) is increasing faster than other neurodegenerative disorders. Neuropathologically, PD is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta due to the accumulation of aggregates of misfolded α-synuclein (α-Syn) in the cytoplasm of these neurons, forming Lewy bodies. Extracellular vesicles (EVs) are associated with the spread of α-Syn to different brain areas. However, at the same time that these EVs contribute to the pathophysiology of PD, they can also be explored as therapeutic, serving as a vehicle to deliver specific molecules, since these vesicles can easily cross the blood-brain barrier. Thus, this review summarizes the recent progress in EVs as a therapeutic strategy for PD, focusing on their delivery to the brain, and discusses the potential challenges and future directions in this field.
[Names] => Michelli Ramires Teixeira ... Rodrigo Pinheiro Araldi [Doi] => 10.37349/en.2023.00016 [Published] => June 29, 2023 [Viewed] => 974 [Downloaded] => 34 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00016 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 76 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:106–122 [Recommend] => 0 [Keywords] => Parkinson’s disease, extracellular vesicles, exosome, drug delivery [DetailTitle] => Extracellular Vesicles as Cell-based Therapeutics [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/76 [Id] => 100616 [ris] => https://www.explorationpub.com/uploads/Article/A100616/068fe380bae0027b2a088d5af70a3017.ris [bib] => https://www.explorationpub.com/uploads/Article/A100616/84c00f5b2075dac08cb08cc5f8929c44.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-26 [CitethisArticle] => Teixeira MR, Alievi AL, da Costa VR, Dias Pinto JR, Araldi RP. Therapeutic potential of extracellular vesicles in Parkinson’s disease. Explor Neurosci. 2023;2:106–22. https://doi.org/10.37349/en.2023.00016 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-06-29 06:12:59 [Bib_Time] => 2023-06-29 06:12:59 [KeysWordContens] => Therapeutic potential of extracellular vesicles in Parkinson’s disease, Parkinson’s disease, extracellular vesicles, exosome, drug delivery, Globally, the incidence of Parkinson’s disease (PD) is increasing faster than other neurodegenerative disorders. Neuropathologically, PD is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta due to the accumulation of aggregates of misfolded α-synuclein (α-Syn) in the cytoplasm of these neurons, forming Lewy bodies. Extracellular vesicles (EVs) are associated with the spread of α-Syn to different brain areas. However, at the same time that these EVs contribute to the pathophysiology of PD, they can also be explored as therapeutic, serving as a vehicle to deliver specific molecules, since these vesicles can easily cross the blood-brain barrier. Thus, this review summarizes the recent progress in EVs as a therapeutic strategy for PD, focusing on their delivery to the brain, and discusses the potential challenges and future directions in this field. ,Michelli Ramires Teixeira ... Rodrigo Pinheiro Araldi [PublishedText] => Published [IsEdit] => 0 [AccountId] => 55 [Zh] => 1 ) [16] => Array ( [ArticleId] => 641 [Create_Time] => 2023-06-30 [zipUrl] => https://www.explorationpub.com/uploads/zip/202307/20230703023007.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100617/100617.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100617/100617.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100617/100617_cover.png [JournalsId] => 8 [Title] => Circadian regulation of the immune-hematopoietic system [Abstract] => Earth’s rotation generates the basic circadian rhythm of day and night to which all living organisms must adapt to survive. In mammals, this happens thanks to a central clock located in the suprac [AbstractComplete] =>Earth’s rotation generates the basic circadian rhythm of day and night to which all living organisms must adapt to survive. In mammals, this happens thanks to a central clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus and to peripheral clock genes at the cellular level. The main environmental cue capable of synchronizing such clocks is light sensed by retinal ganglion cells signaling through a complex nervous pathway to the pineal gland which ultimately regulates melatonin synthesis that occurs during the night, darkness hours in all mammals. The central clock synchronized by melatonin drives the circadian oscillation of the sympathetic nervous system (SNS) adrenergic activity which in turn controls glucocorticoid production in the adrenal glands. These oscillations are integrated with peripheral cellular clocks by still not completely understood mechanisms and drive the homeostatic control of activity-rest (sleep) cycles, cardiovascular activity, body temperature, and immune-hematopoietic functions. The neuronal and hormonal mechanisms governing the circadian oscillation of hematopoiesis and immunity will be addressed in this review focusing on those offering therapeutic perspectives.
[Names] => Georges Maestroni [Doi] => 10.37349/en.2023.00017 [Published] => June 30, 2023 [Viewed] => 964 [Downloaded] => 38 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00017 [Inline] => 1 [Type] => 1 [Issue] => 3 [Topic] => 82 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:123–139 [Recommend] => 0 [Keywords] => Suprachiasmatic nucleus, melatonin, clock genes, circadian rhythm, hematopoiesis, immune response [DetailTitle] => Circadian Rhythm and Melatonin [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/82 [Id] => 100617 [ris] => https://www.explorationpub.com/uploads/Article/A100617/7d6e762945850a43fcb9b7673d8afccc.ris [bib] => https://www.explorationpub.com/uploads/Article/A100617/501d3a4fe01ce3089890e4cca9f1cc62.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-27 [CitethisArticle] => Maestroni G. Circadian regulation of the immune-hematopoietic system. Explor Neurosci. 2023;2:123–39. https://doi.org/10.37349/en.2023.00017 [Jindex] => 0 [CName] => GeorgesMaestroni, [CEmail] => georges.maestroni@tim.it, [Ris_Time] => 2023-06-30 05:41:25 [Bib_Time] => 2023-06-30 05:41:25 [KeysWordContens] => Circadian regulation of the immune-hematopoietic system, Suprachiasmatic nucleus, melatonin, clock genes, circadian rhythm, hematopoiesis, immune response, Earth’s rotation generates the basic circadian rhythm of day and night to which all living organisms must adapt to survive. In mammals, this happens thanks to a central clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus and to peripheral clock genes at the cellular level. The main environmental cue capable of synchronizing such clocks is light sensed by retinal ganglion cells signaling through a complex nervous pathway to the pineal gland which ultimately regulates melatonin synthesis that occurs during the night, darkness hours in all mammals. The central clock synchronized by melatonin drives the circadian oscillation of the sympathetic nervous system (SNS) adrenergic activity which in turn controls glucocorticoid production in the adrenal glands. These oscillations are integrated with peripheral cellular clocks by still not completely understood mechanisms and drive the homeostatic control of activity-rest (sleep) cycles, cardiovascular activity, body temperature, and immune-hematopoietic functions. The neuronal and hormonal mechanisms governing the circadian oscillation of hematopoiesis and immunity will be addressed in this review focusing on those offering therapeutic perspectives. ,Georges Maestroni [PublishedText] => Published [IsEdit] => 0 [AccountId] => 48 [Zh] => 1 ) [17] => Array ( [ArticleId] => 751 [Create_Time] => 2023-08-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230830073351.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100618/100618.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100618/100618.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100618/100618_cover.png [JournalsId] => 8 [Title] => Modify gut microbiome in autism: a promising strategy? [Abstract] => The gut microbiota and dysbiosis have been implicated in various metabolic diseases and gastrointestinal disorders. Recently, there has been growing evidence suggesting the influence of gut microbio [AbstractComplete] =>The gut microbiota and dysbiosis have been implicated in various metabolic diseases and gastrointestinal disorders. Recently, there has been growing evidence suggesting the influence of gut microbiota on neurological disorders, including autism. Although the number of children diagnosed with autism is increasing, the exact cause of the disease remains unknown. Numerous factors, such as genetics, environment, and diet, appear to contribute to its onset. Nevertheless, a degree of general consensus exists regarding the notion that the disease’s progression likely demands the participation of multiple factors. Among the potential causes, the role of the microbiota is particularly intriguing. The gut and brain have extensive connections, with a significant number of neuronal cells in the gut, and autism is often associated with gastrointestinal issues. In this review, the most recent information available on autism and microbiota has been analyzed. Findings of this study indicate that: (1) the microbiota is clearly altered in individuals with autism spectrum disorder (ASD); (2) microbiota transplantation appears to be effective in reducing the severity of autism symptoms; (3) while the microbiota is not solely responsible for the onset of autism, it likely plays a significant role. Considering all the available information, it is suggested that modifying the gut microbiota may have a positive impact on individuals with autism. This opens up possibilities for the use of pre- or probiotics in the treatment of children with ASD, as well as the potential use of fecal microbiota transfer.
[Names] => Jean Demarquoy ... Caroline Demarquoy [Doi] => 10.37349/en.2023.00018 [Published] => August 31, 2023 [Viewed] => 612 [Downloaded] => 22 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00018 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 0 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:140–152 [Recommend] => 0 [Keywords] => Autism spectrum disorder, microbiota, fecal microbiota transplantation, bacteria, etiology [DetailTitle] => [DetailUrl] => [Id] => 100618 [ris] => https://www.explorationpub.com/uploads/Article/A100618/716e11b3efe5a7061b017a1aa9d2a8c3.ris [bib] => https://www.explorationpub.com/uploads/Article/A100618/c11e79e7e8c07314c5dd4979896eb5c2.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Demarquoy J, Othman H, Demarquoy C. Modify gut microbiome in autism: a promising strategy? Explor Neurosci. 2023;2:140–52. https://doi.org/10.37349/en.2023.00018 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-30 07:33:52 [Bib_Time] => 2023-08-30 07:33:52 [KeysWordContens] => Modify gut microbiome in autism: a promising strategy?, Autism spectrum disorder, microbiota, fecal microbiota transplantation, bacteria, etiology, The gut microbiota and dysbiosis have been implicated in various metabolic diseases and gastrointestinal disorders. Recently, there has been growing evidence suggesting the influence of gut microbiota on neurological disorders, including autism. Although the number of children diagnosed with autism is increasing, the exact cause of the disease remains unknown. Numerous factors, such as genetics, environment, and diet, appear to contribute to its onset. Nevertheless, a degree of general consensus exists regarding the notion that the disease’s progression likely demands the participation of multiple factors. Among the potential causes, the role of the microbiota is particularly intriguing. The gut and brain have extensive connections, with a significant number of neuronal cells in the gut, and autism is often associated with gastrointestinal issues. In this review, the most recent information available on autism and microbiota has been analyzed. Findings of this study indicate that: (1) the microbiota is clearly altered in individuals with autism spectrum disorder (ASD); (2) microbiota transplantation appears to be effective in reducing the severity of autism symptoms; (3) while the microbiota is not solely responsible for the onset of autism, it likely plays a significant role. Considering all the available information, it is suggested that modifying the gut microbiota may have a positive impact on individuals with autism. This opens up possibilities for the use of pre- or probiotics in the treatment of children with ASD, as well as the potential use of fecal microbiota transfer. ,Jean Demarquoy ... Caroline Demarquoy [PublishedText] => Published [IsEdit] => 0 [AccountId] => 77 [Zh] => 1 ) [18] => Array ( [ArticleId] => 756 [Create_Time] => 2023-08-31 [zipUrl] => https://www.explorationpub.com/uploads/zip/202309/20230907013547.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100619/100619.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100619/100619.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100619/100619_cover.png [JournalsId] => 8 [Title] => Covered stent graft for treatment of carotid artery stenosis with post-stenotic aneurysm [Abstract] => Several bare metals, self-expanding stents have been approved by the Food and Drug Administration (FDA) to treat carotid stenosis, but no covered stents have been particularly examined or approved f [AbstractComplete] =>Several bare metals, self-expanding stents have been approved by the Food and Drug Administration (FDA) to treat carotid stenosis, but no covered stents have been particularly examined or approved for carotid or cerebrovascular applications. Nonetheless, there are a number of potentially useful applications for covered stents in the brachiocephalic, carotid, and even intracranial arteries. As with currently accepted applications for bare metal carotid stents, the use of covered stents in carotid arteries has been reserved for patients who are at high risk for complications with open surgical management of their specific problem. The present case report emphasizes the safety and efficacy of covered stent in complex carotid artery reconstruction entailing stenosis and aneurysmal dilatation and through light on its impact on minimizing the risk of ischemic complications associated with endovascular or surgical carotid sacrifice.
[Names] => Mosaad Soliman ... Reem Soliman [Doi] => 10.37349/en.2023.00019 [Published] => August 31, 2023 [Viewed] => 508 [Downloaded] => 16 [Subject] => Case Report [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00019 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 0 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:153–159 [Recommend] => 0 [Keywords] => Carotid artery stenosis, covered stent graft, internal carotid artery stenting, post-stenotic dilatation [DetailTitle] => [DetailUrl] => [Id] => 100619 [ris] => https://www.explorationpub.com/uploads/Article/A100619/a6a7272e4f1475fcb3e8c7af8cf21582.ris [bib] => https://www.explorationpub.com/uploads/Article/A100619/96f0d4762b4441b389e02db47231fc97.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Soliman M, Mowafy K, Elgwad MA, Soliman R, Soliman R. Covered stent graft for treatment of carotid artery stenosis with post-stenotic aneurysm. Explor Neurosci. 2023;2:153–9. https://doi.org/10.37349/en.2023.00019 [Jindex] => 0 [CName] => MosaadSoliman, [CEmail] => Soliman_mosaad@hotmail.com, [Ris_Time] => 2023-08-29 05:48:33 [Bib_Time] => 2023-08-29 06:29:48 [KeysWordContens] => Covered stent graft for treatment of carotid artery stenosis with post-stenotic aneurysm, Carotid artery stenosis, covered stent graft, internal carotid artery stenting, post-stenotic dilatation, Several bare metals, self-expanding stents have been approved by the Food and Drug Administration (FDA) to treat carotid stenosis, but no covered stents have been particularly examined or approved for carotid or cerebrovascular applications. Nonetheless, there are a number of potentially useful applications for covered stents in the brachiocephalic, carotid, and even intracranial arteries. As with currently accepted applications for bare metal carotid stents, the use of covered stents in carotid arteries has been reserved for patients who are at high risk for complications with open surgical management of their specific problem. The present case report emphasizes the safety and efficacy of covered stent in complex carotid artery reconstruction entailing stenosis and aneurysmal dilatation and through light on its impact on minimizing the risk of ischemic complications associated with endovascular or surgical carotid sacrifice. ,Mosaad Soliman ... Reem Soliman [PublishedText] => Published [IsEdit] => 0 [AccountId] => 76 [Zh] => 1 ) [19] => Array ( [ArticleId] => 775 [Create_Time] => 2023-09-01 [zipUrl] => https://www.explorationpub.com/uploads/zip/202308/20230831085834.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100620/100620.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100620/100620.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100620/100620_cover.png [JournalsId] => 8 [Title] => Multiple sclerosis with comorbidity depression and its association with vitamin D deficiency in a narrative review of the current literature [Abstract] => Over the past decade, knowledge of the pathophysiology and immunology of multiple sclerosis (MS) and depression, and the complex links to vitamin D (VitD) balance, has increased rapidly. Both diseas [AbstractComplete] =>Over the past decade, knowledge of the pathophysiology and immunology of multiple sclerosis (MS) and depression, and the complex links to vitamin D (VitD) balance, has increased rapidly. Both diseases are characterized by an imbalance of proinflammatory and antiinflammatory cytokines, increased serum neurofilament light chains (sNfLs), disruption of the blood-brain barrier (BBB), abolition of the physiological function of the various types of microglia (MG), decreased calcidiol-serum levels, and disorders of the gut microbiome in combination with hyperactivity of the hypothalamic-pituitary-adrenal (HPA)-axis/microbiome-gut-brain-axis characterized. In depression, stress initiates cellular and molecular changes in the brain via increased cortisol release in the HPA-axis. Microglial activation and neuronal damage as well as dysregulation of neuroplastic and neurotrophic factors complete the spectrum of pathological damage. It is shown that gut dysbiosis leads to increased gut permeability, which favors endotoxemia and ultimately paves the way to systemic inflammation. A VitD supplementation could restore the balance of microorganisms in the intestine and reduce the inflammatory processes at various levels. VitD promotes regulatory T cell (Treg) proliferation, inhibits the expression of T helper 1 (Th1) cells and Th17 immune cells, and inhibits proinflammatory interleukin-17 (IL-17). 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] reduces also the secretion of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). Increased calcitriol levels lead to a reduction in MG activation, oxidative stress, and lower BBB permeability. An early, permanent, daily sufficient VitD supplementation as an add-on therapy under control of the serum 25-hydroxyvitamin D [s25(OH)D] levels is an essential therapeutic tool to slow down the disability caused by MS and thereby primarily prevent or reduce the stress and subsequently the manifestation of depression. Through the future continuous measurement of the biomarkers serum neurofilament ligth chains and glial fibrillary acidic proteins as well as the s25(OH)D level in MS and comorbidity depression, future therapy successes or failures can be avoided.
[Names] => Hans-Klaus Goischke [Doi] => 10.37349/en.2023.00020 [Published] => August 31, 2023 [Viewed] => 761 [Downloaded] => 22 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00020 [Inline] => 1 [Type] => 1 [Issue] => 4 [Topic] => 153 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:160–192 [Recommend] => 0 [Keywords] => Depression, multiple sclerosis, pathophysiology, immunology, vitamin D supplementation, 25-hydroxyvitamin D levels, serum neurofilament light chains [DetailTitle] => Novel Therapeutic Approaches for the Treatment of Depression [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/153 [Id] => 100620 [ris] => https://www.explorationpub.com/uploads/Article/A100620/3078a532831a2881c951deb1c93d15ee.ris [bib] => https://www.explorationpub.com/uploads/Article/A100620/9b28fbdc04b70fe1de7128605b5649bd.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Goischke HK. Multiple sclerosis with comorbidity depression and its association with vitamin D deficiency in a narrative review of the current literature. Explor Neurosci. 2023;2:160–92. https://doi.org/10.37349/en.2023.00020 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-08-30 07:17:08 [Bib_Time] => 2023-08-30 07:17:08 [KeysWordContens] => Multiple sclerosis with comorbidity depression and its association with vitamin D deficiency in a narrative review of the current literature, Depression, multiple sclerosis, pathophysiology, immunology, vitamin D supplementation, 25-hydroxyvitamin D levels, serum neurofilament light chains, Over the past decade, knowledge of the pathophysiology and immunology of multiple sclerosis (MS) and depression, and the complex links to vitamin D (VitD) balance, has increased rapidly. Both diseases are characterized by an imbalance of proinflammatory and antiinflammatory cytokines, increased serum neurofilament light chains (sNfLs), disruption of the blood-brain barrier (BBB), abolition of the physiological function of the various types of microglia (MG), decreased calcidiol-serum levels, and disorders of the gut microbiome in combination with hyperactivity of the hypothalamic-pituitary-adrenal (HPA)-axis/microbiome-gut-brain-axis characterized. In depression, stress initiates cellular and molecular changes in the brain via increased cortisol release in the HPA-axis. Microglial activation and neuronal damage as well as dysregulation of neuroplastic and neurotrophic factors complete the spectrum of pathological damage. It is shown that gut dysbiosis leads to increased gut permeability, which favors endotoxemia and ultimately paves the way to systemic inflammation. A VitD supplementation could restore the balance of microorganisms in the intestine and reduce the inflammatory processes at various levels. VitD promotes regulatory T cell (Treg) proliferation, inhibits the expression of T helper 1 (Th1) cells and Th17 immune cells, and inhibits proinflammatory interleukin-17 (IL-17). 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] reduces also the secretion of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). Increased calcitriol levels lead to a reduction in MG activation, oxidative stress, and lower BBB permeability. An early, permanent, daily sufficient VitD supplementation as an add-on therapy under control of the serum 25-hydroxyvitamin D [s25(OH)D] levels is an essential therapeutic tool to slow down the disability caused by MS and thereby primarily prevent or reduce the stress and subsequently the manifestation of depression. Through the future continuous measurement of the biomarkers serum neurofilament ligth chains and glial fibrillary acidic proteins as well as the s25(OH)D level in MS and comorbidity depression, future therapy successes or failures can be avoided. ,Hans-Klaus Goischke [PublishedText] => Published [IsEdit] => 0 [AccountId] => 72 [Zh] => 1 ) [20] => Array ( [ArticleId] => 825 [Create_Time] => 2023-09-28 [zipUrl] => https://www.explorationpub.com/uploads/zip/202309/20230928062930.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100621/100621.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100621/100621.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100621/100621_cover.png [JournalsId] => 8 [Title] => Negative environmental influences on the developing brain mediated by epigenetic modifications [Abstract] => Brain development, a complex process, consisting of several phases, starting as early as two weeks after conception, and continuing through childhood till early adolescence, is crucial for the devel [AbstractComplete] =>Brain development, a complex process, consisting of several phases, starting as early as two weeks after conception, and continuing through childhood till early adolescence, is crucial for the development of properly functioning body systems, behavioral traits, and neurocognitive abilities. Infancy and childhood are recognized as important periods for initial brain formation, however in later stages of life, such as childhood and adulthood, experiences, together with environmental exposures, can still influence brain physiology. The developing brain is particularly susceptible to epigenetic changes with many factors being proposed as modifiers by directly impacting DNA methylation as well as histone and chromatin modifications within genes implicated in development. These factors include: maternal stress and diet, exposure to pollutants, sleep quality, as well as dietary habits. Evidence indicates exposures to environmental threats can lead to inappropriate neurological, metabolic, and endocrine functioning often mediated by epigenetic mechanisms with symptoms manifesting themselves as early as childhood or in later stages of life. Therefore, the main aim of this review is to evaluate the current studies focused on negative environmental exposures and their consequences on the developing brain directed by epigenetic mechanisms.
[Names] => Maya Komar-Fletcher ... Joanna Michalina Jurek [Doi] => 10.37349/en.2023.00021 [Published] => September 28, 2023 [Viewed] => 977 [Downloaded] => 29 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00021 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 0 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:193–211 [Recommend] => 0 [Keywords] => Environmental factors, epigenetic modifications, brain development, nutrition, maternal factors, sleep quality, neuropsychiatric disorders [DetailTitle] => [DetailUrl] => [Id] => 100621 [ris] => https://www.explorationpub.com/uploads/Article/A100621/86fa2bda5d7116b1193a63fa0c718f06.ris [bib] => https://www.explorationpub.com/uploads/Article/A100621/b011a030ae5652f884164e88f1618174.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Komar-Fletcher M, Wojas J, Rutkowska M, Raczyńska G, Nowacka A, Jurek JM. Negative environmental influences on the developing brain mediated by epigenetic modifications. Explor Neurosci. 2023;2:193–211. https://doi.org/10.37349/en.2023.00021 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-09-26 07:31:01 [Bib_Time] => 2023-09-26 07:31:01 [KeysWordContens] => Negative environmental influences on the developing brain mediated by epigenetic modifications, Environmental factors, epigenetic modifications, brain development, nutrition, maternal factors, sleep quality, neuropsychiatric disorders, Brain development, a complex process, consisting of several phases, starting as early as two weeks after conception, and continuing through childhood till early adolescence, is crucial for the development of properly functioning body systems, behavioral traits, and neurocognitive abilities. Infancy and childhood are recognized as important periods for initial brain formation, however in later stages of life, such as childhood and adulthood, experiences, together with environmental exposures, can still influence brain physiology. The developing brain is particularly susceptible to epigenetic changes with many factors being proposed as modifiers by directly impacting DNA methylation as well as histone and chromatin modifications within genes implicated in development. These factors include: maternal stress and diet, exposure to pollutants, sleep quality, as well as dietary habits. Evidence indicates exposures to environmental threats can lead to inappropriate neurological, metabolic, and endocrine functioning often mediated by epigenetic mechanisms with symptoms manifesting themselves as early as childhood or in later stages of life. Therefore, the main aim of this review is to evaluate the current studies focused on negative environmental exposures and their consequences on the developing brain directed by epigenetic mechanisms. ,Maya Komar-Fletcher ... Joanna Michalina Jurek [PublishedText] => Published [IsEdit] => 0 [AccountId] => 72 [Zh] => 1 ) [21] => Array ( [ArticleId] => 830 [Create_Time] => 2023-10-09 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231009014709.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100622/100622.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100622/100622.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100622/100622_cover.png [JournalsId] => 8 [Title] => Sleep disorders contribute to the development of dementia and Alzheimer’s disease [Abstract] => Life is the highest form of adaptation to the environment which is based on energy metabolism. To maintain life, the neuromuscular system must constantly interact with the environment. The striatal [AbstractComplete] =>Life is the highest form of adaptation to the environment which is based on energy metabolism. To maintain life, the neuromuscular system must constantly interact with the environment. The striatal muscles are the main energy consumer and their access to energy fuel is mainly limited by the brain’s needs. In the state of wakefulness, the brain must continuously process streams of sensory signals and respond to them with motor actions. At the same time, the brain to be efficient must memorize the sensory-movement relationships. Brain memory networking requires additional energy allocation, and due to limited systemic energy resources, the processes of memorization are completed during the sleep phase when the inactive muscular system allows allocating the energy fuel to the brain functions such as memory trace formation and the removal of the activity-dependent waste products. Both physiological processes can be completed during sleep only, and consequently, chronic sleep disorder leads to pathological changes in brain functioning and escalation of neurodegenerative processes. Consequently, sleep disorders become the main cause of dementia which is the prodrome of Alzheimer’s disease.
[Names] => Janusz Wiesław Błaszczyk [Doi] => 10.37349/en.2023.00022 [Published] => October 08, 2023 [Viewed] => 774 [Downloaded] => 19 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00022 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 187 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:212–223 [Recommend] => 0 [Keywords] => Brain physiology, sleep disorders, aging, neurodegeneration [DetailTitle] => Alzheimer’s Disease [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/187 [Id] => 100622 [ris] => https://www.explorationpub.com/uploads/Article/A100622/64d6f760fc14969f1f280bcc297c39b4.ris [bib] => https://www.explorationpub.com/uploads/Article/A100622/2fc0b45931e09859d5769ec1a1cfa225.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Błaszczyk JW. Sleep disorders contribute to the development of dementia and Alzheimer’s disease. Explor Neurosci. 2023;2:212–23. https://doi.org/10.37349/en.2023.00022 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-10-31 05:10:28 [Bib_Time] => 2023-10-31 05:10:28 [KeysWordContens] => Sleep disorders contribute to the development of dementia and Alzheimer’s disease, Brain physiology, sleep disorders, aging, neurodegeneration, Life is the highest form of adaptation to the environment which is based on energy metabolism. To maintain life, the neuromuscular system must constantly interact with the environment. The striatal muscles are the main energy consumer and their access to energy fuel is mainly limited by the brain’s needs. In the state of wakefulness, the brain must continuously process streams of sensory signals and respond to them with motor actions. At the same time, the brain to be efficient must memorize the sensory-movement relationships. Brain memory networking requires additional energy allocation, and due to limited systemic energy resources, the processes of memorization are completed during the sleep phase when the inactive muscular system allows allocating the energy fuel to the brain functions such as memory trace formation and the removal of the activity-dependent waste products. Both physiological processes can be completed during sleep only, and consequently, chronic sleep disorder leads to pathological changes in brain functioning and escalation of neurodegenerative processes. Consequently, sleep disorders become the main cause of dementia which is the prodrome of Alzheimer’s disease. ,Janusz Wiesław Błaszczyk [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [22] => Array ( [ArticleId] => 846 [Create_Time] => 2023-10-16 [zipUrl] => https://www.explorationpub.com/uploads/zip/202310/20231030081035.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100623/100623.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100623/100623.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100623/100623_cover.png [JournalsId] => 8 [Title] => Investigation into the vascular contributors to dementia and the associated treatments [Abstract] => As the average lifespan has increased, memory disorders have become a more pressing public health concern. However, dementia in the elderly population is often neglected in light of other health pri [AbstractComplete] =>As the average lifespan has increased, memory disorders have become a more pressing public health concern. However, dementia in the elderly population is often neglected in light of other health priorities. Therefore, expanding the knowledge surrounding the pathology of dementia will allow more informed decision-making regarding treatment within elderly and older adult populations. An important emerging avenue in dementia research is understanding the vascular contributors to dementia. This review summarizes potential causes of vascular cognitive impairment like stroke, microinfarction, hypertension, atherosclerosis, blood-brain barrier dysfunction, and cerebral amyloid angiopathy. Also, this review address treatments that target these vascular impairments that also show promising results in reducing patient’s risk for and experience of dementia.
[Names] => Caroline Grace Davidson ... Brandon Lucke-Wold [Doi] => 10.37349/en.2023.00023 [Published] => October 15, 2023 [Viewed] => 821 [Downloaded] => 27 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00023 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 115 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:224–237 [Recommend] => 0 [Keywords] => Dementia, vascular contributors, microinfarction, amyloid [DetailTitle] => Emerging Trends in Endovascular Management [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/115 [Id] => 100623 [ris] => https://www.explorationpub.com/uploads/Article/A100623/bbc776a4dd3c2f550482acb0e54fe259.ris [bib] => https://www.explorationpub.com/uploads/Article/A100623/9c74edb3157447904446ed33569d04b4.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-27 [CitethisArticle] => Davidson CG, Woodford SJ, Mathur S, Valle DB, Foster D, Kioutchoukova I, et al. Investigation into the vascular contributors to dementia and the associated treatments. Explor Neurosci. 2023;2:224–37. https://doi.org/10.37349/en.2023.00023 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-10-13 02:28:05 [Bib_Time] => 2023-10-13 02:28:05 [KeysWordContens] => Investigation into the vascular contributors to dementia and the associated treatments, Dementia, vascular contributors, microinfarction, amyloid, As the average lifespan has increased, memory disorders have become a more pressing public health concern. However, dementia in the elderly population is often neglected in light of other health priorities. Therefore, expanding the knowledge surrounding the pathology of dementia will allow more informed decision-making regarding treatment within elderly and older adult populations. An important emerging avenue in dementia research is understanding the vascular contributors to dementia. This review summarizes potential causes of vascular cognitive impairment like stroke, microinfarction, hypertension, atherosclerosis, blood-brain barrier dysfunction, and cerebral amyloid angiopathy. Also, this review address treatments that target these vascular impairments that also show promising results in reducing patient’s risk for and experience of dementia. ,Caroline Grace Davidson ... Brandon Lucke-Wold [PublishedText] => Published [IsEdit] => 0 [AccountId] => 56 [Zh] => 1 ) [23] => Array ( [ArticleId] => 847 [Create_Time] => 2023-10-16 [zipUrl] => https://www.explorationpub.com/uploads/zip/202311/20231101013421.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100624/100624.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100624/100624.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100624/100624_cover.png [JournalsId] => 8 [Title] => Estimation of the allelic status of apolipoprotein E4 isoforms with fully automated LUMIPULSE® assays [Abstract] => Aim: Apolipoprotein E (ApoE) isoforms, especially the ApoE4 isoform, are genetic risk factors for Alzheimer’s disease (AD). Moreover, the APOE ε4 haplotype has a dose-dependent association wit [AbstractComplete] =>Apolipoprotein E (ApoE) isoforms, especially the ApoE4 isoform, are genetic risk factors for Alzheimer’s disease (AD). Moreover, the APOE ε4 haplotype has a dose-dependent association with an increased risk of amyloid-related imaging abnormalities (ARIA) in individuals receiving disease-modifying therapy for AD. Therefore, the importance of APOE genotyping or proteotyping has been highlighted. Here, the authors developed fully automated chemiluminescence enzyme-immunoassay kit for ApoE4 and Pan-ApoE, and evaluated their diagnostic concordance with the APOE genotyping.
One hundred seventy-eight specimens were analyzed using the Lumipulse® G ApoE4 and Pan-ApoE for the ApoE proteotype and evaluated its diagnostic concordance with the APOE genotype.
The ApoE4 kit specifically detected the ApoE4 concentration in plasma samples, and the polymorphism could be classified clearly by the ratio of ApoE4 and Pan-ApoE amount in plasma.
The combination of Pan-ApoE and ApoE4-specific chemiluminescent enzyme immunoassay (CLEIA) assay is useful for predicting APOE ε4 allele status.
The two mainstays of therapy for refractory epilepsy are medication and surgery. Child behavioral and cognitive aspects of epilepsy can be improved by using a specialized dietary regimen such as the ketogenic diet (KD). The purpose of this review is to expand our understanding of KD as a nutritional therapy for children with refractory epilepsy and to provide insight into the physiological aspects of its efficacy as an alternative to anti-seizure medication. Either directly or indirectly, ketones, glucose restriction, and polyunsaturated fatty acids regulate epileptic seizures. For KD to be effective, all three of these components must be present, even though the exact mechanism is unknown. Increasing gamma-aminobutyric acid, mitochondrial biogenesis, and oxidative phosphorylation levels can also serve as a means of promoting stable synaptic function while also decreasing neural activity and excitability. Most side effects of KD are caused by mild metabolic abnormalities such as acidosis, hyperuricemia, hypercholesterolemia, hypocalcemia, and hypomagnesemia. Since medium-chain triglycerides (MCTs) produce more ketones per calorie than long-chain triglycerides, individuals who consume MCTs can consume more carbohydrates and protein. This review demonstrated that KD therapy led to positive outcomes for patients with refractory epilepsy. Further study is needed to evaluate whether less restrictive and easier-to-follow diets, such as the modified Atkins diet and MCT diets, have a similar effect on seizure treatment as the standard KD.
[Names] => Srilaxmi Vityala ... Swathi Nenavath [Doi] => 10.37349/en.2023.00025 [Published] => October 30, 2023 [Viewed] => 2402 [Downloaded] => 614 [Subject] => Mini Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00025 [Inline] => 1 [Type] => 1 [Issue] => 5 [Topic] => 225 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:245–250 [Recommend] => 0 [Keywords] => Ketogenic diet, refractory epilepsy, ketone bodies, medium-chain triglycerides, modified Atkins diet [DetailTitle] => Epilepsy [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/225 [Id] => 100625 [ris] => https://www.explorationpub.com/uploads/Article/A100625/ba6ddf8f44c627df952b819e0609f3c1.ris [bib] => https://www.explorationpub.com/uploads/Article/A100625/5ce25b0cf87337a51c74922177dc2fd3.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Vityala S, Kanteti KP, Abdul HM, Vityala Y, Damineni U, Bellam S, et al. Nutritional treatment with the ketogenic diet in children with refractory epilepsy: a narrative review. Explor Neurosci. 2023;2:245–50. https://doi.org/10.37349/en.2023.00025 [Jindex] => 0 [CName] => YethindraVityala, [CEmail] => yethindravityala10@gmail.com, [Ris_Time] => 2023-10-27 08:49:07 [Bib_Time] => 2023-10-27 08:49:07 [KeysWordContens] => Nutritional treatment with the ketogenic diet in children with refractory epilepsy: a narrative review, Ketogenic diet, refractory epilepsy, ketone bodies, medium-chain triglycerides, modified Atkins diet, The two mainstays of therapy for refractory epilepsy are medication and surgery. Child behavioral and cognitive aspects of epilepsy can be improved by using a specialized dietary regimen such as the ketogenic diet (KD). The purpose of this review is to expand our understanding of KD as a nutritional therapy for children with refractory epilepsy and to provide insight into the physiological aspects of its efficacy as an alternative to anti-seizure medication. Either directly or indirectly, ketones, glucose restriction, and polyunsaturated fatty acids regulate epileptic seizures. For KD to be effective, all three of these components must be present, even though the exact mechanism is unknown. Increasing gamma-aminobutyric acid, mitochondrial biogenesis, and oxidative phosphorylation levels can also serve as a means of promoting stable synaptic function while also decreasing neural activity and excitability. Most side effects of KD are caused by mild metabolic abnormalities such as acidosis, hyperuricemia, hypercholesterolemia, hypocalcemia, and hypomagnesemia. Since medium-chain triglycerides (MCTs) produce more ketones per calorie than long-chain triglycerides, individuals who consume MCTs can consume more carbohydrates and protein. This review demonstrated that KD therapy led to positive outcomes for patients with refractory epilepsy. Further study is needed to evaluate whether less restrictive and easier-to-follow diets, such as the modified Atkins diet and MCT diets, have a similar effect on seizure treatment as the standard KD. ,Srilaxmi Vityala ... Swathi Nenavath [PublishedText] => Published [IsEdit] => 0 [AccountId] => 72 [Zh] => 1 ) [25] => Array ( [ArticleId] => 976 [Create_Time] => 2023-12-06 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231204085412.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100626/100626.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100626/100626.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100626/100626_cover.png [JournalsId] => 8 [Title] => Stigma and psychosocial problems in patients with epilepsy [Abstract] => Epilepsy, a prevalent neurological disorder, is characterized by chronic seizures resulting from abnormal electrical activity in the brain. Adequate medical treatment allows roughly 70% of patients [AbstractComplete] =>Epilepsy, a prevalent neurological disorder, is characterized by chronic seizures resulting from abnormal electrical activity in the brain. Adequate medical treatment allows roughly 70% of patients to enjoy a seizure-free life. However, throughout history, epilepsy has acquired diverse interpretations due to the experienced seizures, transforming the condition from a clinical issue into a social stigma. Therefore, the aim of this review study is to review stigma and psychosocial problems in patients with epilepsy (PwE). For this reason, this study utilises sources from the last ten years and reports current data. As a result of the review, it was found that societal discrimination in PwE arises primarily from inadequate knowledge, misconceptions, and negative attitudes toward the condition. Other contributing factors were include patients’ lower levels of education and income, frequent seizures due to inadequate treatment, age at onset, duration of the disease, depressive symptoms, and lack of social support. Also, it was found that the stigma individuals with epilepsy face plays a pivotal role in exacerbating their psychosocial problems. Unfortunately, stigma and psychosocial challenges appear to be in a vicious circle, with an increase in one increasing the other. Stigmatized patients tended to isolate themselves from society, further increasing their likelihood of experiencing a depressive mood or psychiatric comorbidity. Consequently, individuals with epilepsy encounter difficulties in various domains such as marriage, work, education, and personal life. Considering these significant psychosocial burdens, it is essential to recognize that epilepsy surpasses its medical implications. Unfortunately, current efforts to reduce stigma remain insufficient, necessitating urgent and comprehensive measures to address this issue.
[Names] => Kubra Yeni [Doi] => 10.37349/en.2023.00026 [Published] => December 06, 2023 [Viewed] => 1017 [Downloaded] => 30 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00026 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 225 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:251–263 [Recommend] => 0 [Keywords] => Epilepsy, stigma, psychosocial problems, knowledge, attitude [DetailTitle] => Epilepsy [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/225 [Id] => 100626 [ris] => https://www.explorationpub.com/uploads/Article/A100626/1234c74f3b5a749f4861d102563d3112.ris [bib] => https://www.explorationpub.com/uploads/Article/A100626/9b1a2380ed858830520dbd2d959fc902.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-27 [CitethisArticle] => Yeni K. Stigma and psychosocial problems in patients with epilepsy. Explor Neurosci. 2023;2:251–63. https://doi.org/10.37349/en.2023.00026 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-12-01 05:59:48 [Bib_Time] => 2023-12-01 05:59:48 [KeysWordContens] => Stigma and psychosocial problems in patients with epilepsy, Epilepsy, stigma, psychosocial problems, knowledge, attitude, Epilepsy, a prevalent neurological disorder, is characterized by chronic seizures resulting from abnormal electrical activity in the brain. Adequate medical treatment allows roughly 70% of patients to enjoy a seizure-free life. However, throughout history, epilepsy has acquired diverse interpretations due to the experienced seizures, transforming the condition from a clinical issue into a social stigma. Therefore, the aim of this review study is to review stigma and psychosocial problems in patients with epilepsy (PwE). For this reason, this study utilises sources from the last ten years and reports current data. As a result of the review, it was found that societal discrimination in PwE arises primarily from inadequate knowledge, misconceptions, and negative attitudes toward the condition. Other contributing factors were include patients’ lower levels of education and income, frequent seizures due to inadequate treatment, age at onset, duration of the disease, depressive symptoms, and lack of social support. Also, it was found that the stigma individuals with epilepsy face plays a pivotal role in exacerbating their psychosocial problems. Unfortunately, stigma and psychosocial challenges appear to be in a vicious circle, with an increase in one increasing the other. Stigmatized patients tended to isolate themselves from society, further increasing their likelihood of experiencing a depressive mood or psychiatric comorbidity. Consequently, individuals with epilepsy encounter difficulties in various domains such as marriage, work, education, and personal life. Considering these significant psychosocial burdens, it is essential to recognize that epilepsy surpasses its medical implications. Unfortunately, current efforts to reduce stigma remain insufficient, necessitating urgent and comprehensive measures to address this issue. ,Kubra Yeni [PublishedText] => Published [IsEdit] => 0 [AccountId] => 22 [Zh] => 1 ) [26] => Array ( [ArticleId] => 987 [Create_Time] => 2023-12-14 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231214034511.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100627/100627.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100627/100627.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100627/100627_cover.png [JournalsId] => 8 [Title] => Carotid endarterectomy compared with carotid artery stenting for extracranial carotid artery stenosis: a retrospective single-centre study [Abstract] => Aim: One of the main risk factors for an ischemic stroke is significant carotid artery stenosis, and extracranial severe carotid artery stenosis accounts for 20% of ischemic strokes. Prior to the [AbstractComplete] =>One of the main risk factors for an ischemic stroke is significant carotid artery stenosis, and extracranial severe carotid artery stenosis accounts for 20% of ischemic strokes. Prior to the development of carotid artery stenting (CAS), the only effective and reliable treatment for carotid artery stenosis was carotid endarterectomy (CEA). This study compares the results of CAS and CEA in patients with significant carotid artery stenosis.
Between 2018 and 2022, hospital records of all patients who underwent carotid artery revascularization at the institution were retrospectively analyzed. Patients were divided into two groups depending on whether CEA or CAS was performed for carotid revascularization. Propensity score matching was performed to reduce bias by equating the baseline clinical characteristics of the groups. To compare 30-day, 1-year, and long-term outcomes, rates of transient ischemic attack (TIA), myocardial infarction, stroke, all-cause mortality, and composite endpoints were analyzed.
After PSM, 76 patients each in the CEA and CAS groups were compared. The mean age was 69.80 years ± 11.35 years and 121 (80%) were male. The patients were followed up for a mean of 33 months ± 6 months. The incidence of TIA in the perioperative period [9 (12%) vs. 4 (5%); P < 0.05], TIA and composite endpoint at 1-year period [11 (15%) vs. 2 (3%); P < 0.05 and 27 (36%) vs. 16 (21%); P < 0.05, respectively] were significantly higher in the CAS group than in the CEA group. No difference was observed between the groups in the long-term.
There was no noticeable difference between the CEA and CAS groups in the examination of cases with severe carotid artery stenosis in terms of 1-month, and 1-year results (apart from TIA and composite endpoints), or long-term outcomes. Extracranial carotid artery stenosis can be treated safely and effectively also by CAS.
Neuropathic pain is an increasingly common disease affecting millions of individuals worldwide. Refractory pain poses a significant impact on patients’ quality of life, financial and economic stability, and social interaction. Numerous effective modalities for treatment of refractory neuropathic pain are presently available. Currently, many options provide symptomatic treatment but are associated with an unfavorable side effect profile and increased risk of addiction. The present investigation reviews current medical management for refractory neuropathic pain including the use of antidepressants, anticonvulsants, gabapentinoids and opioid therapy, as well as interventional pain procedures such as spinal cord stimulation (SCS) and intrathecal targeted drug delivery. While multidisciplinary management with lifestyle modification and pharmacologic regimens remains at the forefront of treating many of these patients, interventional modalities are growing in popularity and have been demonstrated to be highly efficacious. In this regard, continued understanding of the pathophysiology surrounding refractory neuropathic pain has led to the development of interventional procedures and better outcomes for patients suffering from refractory neuropathic pain. When and if patients fail conservative therapy, interventional techniques are desirable alternatives for pain management. SCS and intrathecal targeted drug delivery are important tools for the treatment of refractory neuropathic pain. In summary, treatment modalities for refractory neuropathic pain are evolving with demonstrated efficacy. This review aims to outline the efficacy of various interventional procedures for refractory neuropathic pain in comparison to traditional drug therapies.
[Names] => Hannah G. Matejowsky ... Alan D. Kaye [Doi] => 10.37349/en.2023.00028 [Published] => December 22, 2023 [Viewed] => 618 [Downloaded] => 17 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00028 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 194 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:276–286 [Recommend] => 0 [Keywords] => Spinal cord stimulation, neuromodulation, pharmacological treatment, neuropathic pain, targeted drug delivery [DetailTitle] => Neuropathic Pain [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/194 [Id] => 100628 [ris] => https://www.explorationpub.com/uploads/Article/A100628/52f8f78c370580b1859f5c46224dfcb5.ris [bib] => https://www.explorationpub.com/uploads/Article/A100628/1fc862cd0b53a927ec66c0eda29fcb89.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Matejowsky HG, Kataria S, Spillers NJ, O’Quin CC, Barrie S, Ahmadzadeh S, et al. Interventional procedures for refractory neuropathic pain. Explor Neurosci. 2023;2:276–86. https://doi.org/10.37349/en.2023.00028 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-12-20 01:39:47 [Bib_Time] => 2023-12-20 01:39:47 [KeysWordContens] => Interventional procedures for refractory neuropathic pain, Spinal cord stimulation, neuromodulation, pharmacological treatment, neuropathic pain, targeted drug delivery, Neuropathic pain is an increasingly common disease affecting millions of individuals worldwide. Refractory pain poses a significant impact on patients’ quality of life, financial and economic stability, and social interaction. Numerous effective modalities for treatment of refractory neuropathic pain are presently available. Currently, many options provide symptomatic treatment but are associated with an unfavorable side effect profile and increased risk of addiction. The present investigation reviews current medical management for refractory neuropathic pain including the use of antidepressants, anticonvulsants, gabapentinoids and opioid therapy, as well as interventional pain procedures such as spinal cord stimulation (SCS) and intrathecal targeted drug delivery. While multidisciplinary management with lifestyle modification and pharmacologic regimens remains at the forefront of treating many of these patients, interventional modalities are growing in popularity and have been demonstrated to be highly efficacious. In this regard, continued understanding of the pathophysiology surrounding refractory neuropathic pain has led to the development of interventional procedures and better outcomes for patients suffering from refractory neuropathic pain. When and if patients fail conservative therapy, interventional techniques are desirable alternatives for pain management. SCS and intrathecal targeted drug delivery are important tools for the treatment of refractory neuropathic pain. In summary, treatment modalities for refractory neuropathic pain are evolving with demonstrated efficacy. This review aims to outline the efficacy of various interventional procedures for refractory neuropathic pain in comparison to traditional drug therapies. ,Hannah G. Matejowsky ... Alan D. Kaye [PublishedText] => Published [IsEdit] => 0 [AccountId] => 87 [Zh] => 1 ) [28] => Array ( [ArticleId] => 1011 [Create_Time] => 2023-12-22 [zipUrl] => https://www.explorationpub.com/uploads/zip/202401/20240103092144.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100629/100629.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100629/100629.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100629/100629-cover.png [JournalsId] => 8 [Title] => Neuropharmacologic modulation of the melatonergic system [Abstract] => The circadian rhythm is a critical system that governs an organism’s functions in alignment with the light-dark cycle. Melatonin release from the pineal gland plays a crucial role in regulating th [AbstractComplete] =>The circadian rhythm is a critical system that governs an organism’s functions in alignment with the light-dark cycle. Melatonin release from the pineal gland plays a crucial role in regulating the internal clock of the body. Multiple neurotransmitter systems in the central nervous system are linked to the release of melatonin. In this review, the relationship between circadian rhythm, melatonin secretion and various neurotransmitter systems are mainly discussed. Serotonin regulates the circadian rhythm through projections from raphe nuclei. Agomelatine is an example of the synergistic interaction between melatonin and serotonin. Melatonergic agents and selective serotonin reuptake inhibitors also exert notable impacts on depression in concomitant use. Dopamine has an inhibitory effect on melatonin release, while melatonin also inhibits dopamine release. This should be taken into account when considering the use of melatonin in Parkinson’s disease. On the contrary, use of melatonin may offer therapeutic advantages for schizophrenia and tardive dyskinesia. The interaction between norepinephrine and melatonin exhibits diurnal variability, with norepinephrine promoting arousal and inhibiting daytime melatonin secretion. Melatonergic neurons also exert a specific protective influence on cholinergic neurons. Interaction between the histaminergic and melatonergic systems is significant, particularly in association with immunity, sleep, and circadian rhythm. Novel ligands with dual-acting properties, interacting with both the histaminergic and melatonergic systems are investigated. Currently, there is a limited number of approved melatonergic agents that primarily demonstrate positive effects in addressing insomnia and depression. However, there is considerable potential in studying new agents that target both the melatonergic and other neurotransmitter systems, which alleviate various conditions, including neurodegenerative diseases, dementia, autoimmune diseases, allergic diseases, epilepsy, and other neuropsychiatric disorders. The ongoing process of developing and evaluating new ligands selectively targeting the melatonergic system remains crucial in understanding the complex relationship between these systems.
[Names] => Utku Aykan ... Canan Uluoglu [Doi] => 10.37349/en.2023.00029 [Published] => December 22, 2023 [Viewed] => 656 [Downloaded] => 20 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00029 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 82 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:287–306 [Recommend] => 0 [Keywords] => Circadian rhythm, neurotransmitter, melatonin, neuropharmacology [DetailTitle] => Circadian Rhythm and Melatonin [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/82 [Id] => 100629 [ris] => https://www.explorationpub.com/uploads/Article/A100629/a43923cdba304546ba66a915319ac227.ris [bib] => https://www.explorationpub.com/uploads/Article/A100629/a499b1b8e4541b96ae2e31b7e8be2774.bib [ens] => [Cited] => 1 [Cited_Time] => 2024-04-27 [CitethisArticle] => Aykan U, Güvel MC, Paykal G, Uluoglu C. Neuropharmacologic modulation of the melatonergic system. Explor Neurosci. 2023;2:287–306. https://doi.org/10.37349/en.2023.00029 [Jindex] => 0 [CName] => CananUluoglu, [CEmail] => culuoglu@yahoo.com, [Ris_Time] => 2023-12-20 08:50:17 [Bib_Time] => 2023-12-20 08:50:17 [KeysWordContens] => Neuropharmacologic modulation of the melatonergic system, Circadian rhythm, neurotransmitter, melatonin, neuropharmacology, The circadian rhythm is a critical system that governs an organism’s functions in alignment with the light-dark cycle. Melatonin release from the pineal gland plays a crucial role in regulating the internal clock of the body. Multiple neurotransmitter systems in the central nervous system are linked to the release of melatonin. In this review, the relationship between circadian rhythm, melatonin secretion and various neurotransmitter systems are mainly discussed. Serotonin regulates the circadian rhythm through projections from raphe nuclei. Agomelatine is an example of the synergistic interaction between melatonin and serotonin. Melatonergic agents and selective serotonin reuptake inhibitors also exert notable impacts on depression in concomitant use. Dopamine has an inhibitory effect on melatonin release, while melatonin also inhibits dopamine release. This should be taken into account when considering the use of melatonin in Parkinson’s disease. On the contrary, use of melatonin may offer therapeutic advantages for schizophrenia and tardive dyskinesia. The interaction between norepinephrine and melatonin exhibits diurnal variability, with norepinephrine promoting arousal and inhibiting daytime melatonin secretion. Melatonergic neurons also exert a specific protective influence on cholinergic neurons. Interaction between the histaminergic and melatonergic systems is significant, particularly in association with immunity, sleep, and circadian rhythm. Novel ligands with dual-acting properties, interacting with both the histaminergic and melatonergic systems are investigated. Currently, there is a limited number of approved melatonergic agents that primarily demonstrate positive effects in addressing insomnia and depression. However, there is considerable potential in studying new agents that target both the melatonergic and other neurotransmitter systems, which alleviate various conditions, including neurodegenerative diseases, dementia, autoimmune diseases, allergic diseases, epilepsy, and other neuropsychiatric disorders. The ongoing process of developing and evaluating new ligands selectively targeting the melatonergic system remains crucial in understanding the complex relationship between these systems. ,Utku Aykan ... Canan Uluoglu [PublishedText] => Published [IsEdit] => 0 [AccountId] => 76 [Zh] => 1 ) [29] => Array ( [ArticleId] => 1019 [Create_Time] => 2023-12-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231226015717.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100630/100630.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100630/100630.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100630/100630_cover.png [JournalsId] => 8 [Title] => Neuroprotective compounds from three common medicinal plants of West Bengal, India: a mini review [Abstract] => Neural disorders refer to conditions of the nervous system due to infection or degeneration of the neurons leading to either neurodegenerative disorder or neuropsychiatric disorder. Some such disord [AbstractComplete] =>Neural disorders refer to conditions of the nervous system due to infection or degeneration of the neurons leading to either neurodegenerative disorder or neuropsychiatric disorder. Some such disorders of the nervous system include Parkinsons’s disease, depression, amnesia, dementia, Alzheimer’s disease, schizophrenia, cerebrovascular impairment, epilepsy, seizure disorders, etc. In conventional medical system, some medicines belonging to the class of psychodelic drugs, sedatives, neurotransmitters, neuro-stimulants, etc. are in extensive use. Unfortunately, most of these drugs either delay the progression of the neural disorder or leave the patient with prominent adverse side effects. Several potent bioactive compounds with neuroprotective potential have been reported from medicinal plants and some of them have been found to be highly effective. Belonging from natural sources, mostly, the plant derived compounds exhibit minimum or no cytotoxicity at a prescribed standardised dose against a particular health ailment. Many such phytocompounds from plant sources with potent neuroprotective activities have been in use in Ayurvedacharya, Unani, and Chinese medicine for ages. The compounds if isolated chemically, modified to make more potent neuroprotective derivatives and utilised to make highly effective neuroprotective pharmaceutical formulations with minimum side effects, may open new revolutionary doorways in neuropharmacology. In this review, it has been briefly discussed about the neuroprotective compounds isolated from certain indigenous plants of West Bengal, India, and their mechanism of action.
[Names] => Suvendu Ghosh ... Debosree Ghosh [Doi] => 10.37349/en.2023.00030 [Published] => December 26, 2023 [Viewed] => 692 [Downloaded] => 25 [Subject] => Mini Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00030 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 215 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:307–317 [Recommend] => 0 [Keywords] => Neuroprotection, phytocompounds, Ayurvedacharya, Alzheimer’s disease, Parkinsons’s disease [DetailTitle] => Medicinal Plants and Bioactive Phytochemicals in Neuroprotection [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/215 [Id] => 100630 [ris] => https://www.explorationpub.com/uploads/Article/A100630/d7bf4b01df6ec552570da8d610e6dbf6.ris [bib] => https://www.explorationpub.com/uploads/Article/A100630/1da07a3b10b3d0f70655af2c865f2ecf.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Ghosh S, Singha PS, Ghosh D. Neuroprotective compounds from three common medicinal plants of West Bengal, India: a mini review. Explor Neurosci. 2023;2:307–17. https://doi.org/10.37349/en.2023.00030 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-12-21 01:59:06 [Bib_Time] => 2023-12-21 03:09:31 [KeysWordContens] => Neuroprotective compounds from three common medicinal plants of West Bengal, India: a mini review, Neuroprotection, phytocompounds, Ayurvedacharya, Alzheimer’s disease, Parkinsons’s disease, Neural disorders refer to conditions of the nervous system due to infection or degeneration of the neurons leading to either neurodegenerative disorder or neuropsychiatric disorder. Some such disorders of the nervous system include Parkinsons’s disease, depression, amnesia, dementia, Alzheimer’s disease, schizophrenia, cerebrovascular impairment, epilepsy, seizure disorders, etc. In conventional medical system, some medicines belonging to the class of psychodelic drugs, sedatives, neurotransmitters, neuro-stimulants, etc. are in extensive use. Unfortunately, most of these drugs either delay the progression of the neural disorder or leave the patient with prominent adverse side effects. Several potent bioactive compounds with neuroprotective potential have been reported from medicinal plants and some of them have been found to be highly effective. Belonging from natural sources, mostly, the plant derived compounds exhibit minimum or no cytotoxicity at a prescribed standardised dose against a particular health ailment. Many such phytocompounds from plant sources with potent neuroprotective activities have been in use in Ayurvedacharya, Unani, and Chinese medicine for ages. The compounds if isolated chemically, modified to make more potent neuroprotective derivatives and utilised to make highly effective neuroprotective pharmaceutical formulations with minimum side effects, may open new revolutionary doorways in neuropharmacology. In this review, it has been briefly discussed about the neuroprotective compounds isolated from certain indigenous plants of West Bengal, India, and their mechanism of action. ,Suvendu Ghosh ... Debosree Ghosh [PublishedText] => Published [IsEdit] => 0 [AccountId] => 87 [Zh] => 1 ) [30] => Array ( [ArticleId] => 1052 [Create_Time] => 2023-12-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231229053859.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100631/100631.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100631/100631.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100631/100631-cover.png [JournalsId] => 8 [Title] => Emerging therapies of hemangioblastomas [Abstract] => Hemangioblastoma are benign, vascularized cranial tumors caused by autosomal dominant inherited von Hippel-Lindau disease or can appear sporadically. This review will investigate current and emergin [AbstractComplete] =>Hemangioblastoma are benign, vascularized cranial tumors caused by autosomal dominant inherited von Hippel-Lindau disease or can appear sporadically. This review will investigate current and emerging treatments for cerebral tumors. It will focus on the current and, more importantly, developing hemangioblastoma treatments. Surgical resectioning and radiotherapy are effective treatment options for cerebral tumors, whereas chemotherapies are not commonly used due to their limited ability to penetrate the blood-brain barrier. Recent chemotherapies have shown promise, but further research is needed to determine the efficacy as a treatment for hemangioblastomas. New advances in brachytherapy and immunotherapy are considered promising treatment options for hemangioblastoma. This review aims to offer valuable insights into the latest developments in hemangioblastoma treatments.
[Names] => Chaitanya Sanghadia ... Brandon Lucke-Wold [Doi] => 10.37349/en.2023.00031 [Published] => December 29, 2023 [Viewed] => 620 [Downloaded] => 16 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00031 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 90 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:318–330 [Recommend] => 0 [Keywords] => Hemangioblastoma, cerebral tumor, von Hippel-Lindau, chemotherapy, radiotherapy, brachytherapy, immunotherapy [DetailTitle] => Cerebral Ischemia, Genetics, Comorbidities, Risk Factors and New Therapeutic Options for Neurorestoration [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/90 [Id] => 100631 [ris] => https://www.explorationpub.com/uploads/Article/A100631/272c753eb4050c880dbc6f88ee91b0e7.ris [bib] => https://www.explorationpub.com/uploads/Article/A100631/4b055ca05a9ca28c8bd09364ae6cbf0b.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Sanghadia C, Martinez ME, McNulty M, Russ E, Woolridge M, Cao DT, et al. Emerging therapies of hemangioblastomas. Explor Neurosci. 2023;2:318–30. https://doi.org/10.37349/en.2023.00031 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-12-27 03:21:55 [Bib_Time] => 2023-12-27 03:21:55 [KeysWordContens] => Emerging therapies of hemangioblastomas, Hemangioblastoma, cerebral tumor, von Hippel-Lindau, chemotherapy, radiotherapy, brachytherapy, immunotherapy, Hemangioblastoma are benign, vascularized cranial tumors caused by autosomal dominant inherited von Hippel-Lindau disease or can appear sporadically. This review will investigate current and emerging treatments for cerebral tumors. It will focus on the current and, more importantly, developing hemangioblastoma treatments. Surgical resectioning and radiotherapy are effective treatment options for cerebral tumors, whereas chemotherapies are not commonly used due to their limited ability to penetrate the blood-brain barrier. Recent chemotherapies have shown promise, but further research is needed to determine the efficacy as a treatment for hemangioblastomas. New advances in brachytherapy and immunotherapy are considered promising treatment options for hemangioblastoma. This review aims to offer valuable insights into the latest developments in hemangioblastoma treatments. ,Chaitanya Sanghadia ... Brandon Lucke-Wold [PublishedText] => Published [IsEdit] => 0 [AccountId] => 76 [Zh] => 1 ) [31] => Array ( [ArticleId] => 1068 [Create_Time] => 2023-12-29 [zipUrl] => https://www.explorationpub.com/uploads/zip/202312/20231229080942.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100632/100632.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100632/100632.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100632/100632_cover.png [JournalsId] => 8 [Title] => Psychology of bipolar depression: revisiting past and present researches, prospects ahead, and moving toward future directions [Abstract] => Bipolar disorder (BD) is a debilitating psychiatric disorder characterized by recurrent depression, mania, and hypomania episodes. The interaction of psychological, neuropsychological, and neurobiol [AbstractComplete] =>Bipolar disorder (BD) is a debilitating psychiatric disorder characterized by recurrent depression, mania, and hypomania episodes. The interaction of psychological, neuropsychological, and neurobiological factors (cognitive, behavioral, and emotional) is implicated in the development and persistence of BD. Accordingly, almost all investigators confirm that BD is the outcome of psychological and genetic interactions. Therefore, researchers should consider various factors in the psychopathology and psychotherapy of BD. This selective review first reviews research on these factors, then points to a variety of therapeutic methods for BD [interpersonal and social rhythm therapy (IPSRT), cognitive behavioral therapy (CBT), dialectical behavior therapy (DBT), mindfulness-based cognitive therapy (MBCT), and family-focused therapy (FFT)], and finally suggested a new comprehensive integrated model for the assessment and therapy of BD.
[Names] => Behrooz Afshari [Doi] => 10.37349/en.2023.00032 [Published] => December 29, 2023 [Viewed] => 683 [Downloaded] => 24 [Subject] => Review [Year] => 2023 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2023.00032 [Inline] => 1 [Type] => 1 [Issue] => 6 [Topic] => 153 [TitleAbbr] => Explor Neurosci. [Pages] => 2023;2:331–349 [Recommend] => 0 [Keywords] => Bipolar disorder, psychological factors, comprehensive integrated model [DetailTitle] => Novel Therapeutic Approaches for the Treatment of Depression [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/153 [Id] => 100632 [ris] => https://www.explorationpub.com/uploads/Article/A100632/19667890dc382d34e789cc147b86437f.ris [bib] => https://www.explorationpub.com/uploads/Article/A100632/57ad9e3837ff248958d3fdd24f9a4ac0.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Afshari B. Psychology of bipolar depression: revisiting past and present researches, prospects ahead, and moving toward future directions. Explor Neurosci. 2023;2:331–49. https://doi.org/10.37349/en.2023.00032 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2023-12-29 01:18:37 [Bib_Time] => 2023-12-29 01:18:37 [KeysWordContens] => Psychology of bipolar depression: revisiting past and present researches, prospects ahead, and moving toward future directions, Bipolar disorder, psychological factors, comprehensive integrated model, Bipolar disorder (BD) is a debilitating psychiatric disorder characterized by recurrent depression, mania, and hypomania episodes. The interaction of psychological, neuropsychological, and neurobiological factors (cognitive, behavioral, and emotional) is implicated in the development and persistence of BD. Accordingly, almost all investigators confirm that BD is the outcome of psychological and genetic interactions. Therefore, researchers should consider various factors in the psychopathology and psychotherapy of BD. This selective review first reviews research on these factors, then points to a variety of therapeutic methods for BD [interpersonal and social rhythm therapy (IPSRT), cognitive behavioral therapy (CBT), dialectical behavior therapy (DBT), mindfulness-based cognitive therapy (MBCT), and family-focused therapy (FFT)], and finally suggested a new comprehensive integrated model for the assessment and therapy of BD. ,Behrooz Afshari [PublishedText] => Published [IsEdit] => 0 [AccountId] => 72 [Zh] => 1 ) [32] => Array ( [ArticleId] => 1103 [Create_Time] => 2024-02-20 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240227030846.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100633/100633.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100633/100633.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100633/100633_cover.png [JournalsId] => 8 [Title] => Connecting the ends: signaling via receptor tyrosine kinases and cytoskeletal degradation in neurodegeneration [Abstract] => Receptor tyrosine kinases (RTKs) are known to perform versatile roles in disease landscapes, which determine the fate of the cell. Although much has been discussed from the perspective of proliferat [AbstractComplete] =>Receptor tyrosine kinases (RTKs) are known to perform versatile roles in disease landscapes, which determine the fate of the cell. Although much has been discussed from the perspective of proliferation, this review focuses on the impact of RTK-mediated signaling and its role in cytoskeletal degradation, the penultimate stage of cellular degeneration. In the case of degenerative diseases such as Alzheimer’s disease (AD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD), age-related macular degeneration (AMD), and type 2 diabetes mellitus (T2DM), RTK signaling has been reported to be perturbed in several studies. The implications of downstream signaling via these receptors through canonical and noncanonical pathways alter the status of actin filaments that provide structural integrity to cells. Degenerative signaling leads to the altered status of rat sarcoma (Ras), Ras homologous (Rho), Ras-related C3 botulinum toxin substrate (Rac), and cell division control protein 42 (Cdc42), the best-characterized components of the cytoskeleton remodeling machinery. RTKs, along with their diverse adaptor partners and other membrane receptors, affect the functionality of Rho family guanosine triphosphate hydrolases (GTPases), which are discussed in this review. To conclude, this review focuses on therapeutic strategies targeting RTKs and Rho GTPase-mediated pathways that can be more effective due to their combined multifactorial impact on neurodegenerative cascades.
[Names] => Priyanka Sengupta ... Debashis Mukhopadhyay [Doi] => 10.37349/en.2024.00033 [Published] => February 20, 2024 [Viewed] => 610 [Downloaded] => 23 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2024.00033 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 187 [TitleAbbr] => Explor Neurosci. [Pages] => 2024;3:1–26 [Recommend] => 0 [Keywords] => Receptor tyrosine kinase signaling, nuclear translocation, cytoskeletal remodeling, crosstalk, Rho GTPases, neurodegeneration, Rho/Rac/Cdc42 [DetailTitle] => Alzheimer’s Disease [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/187 [Id] => 100633 [ris] => https://www.explorationpub.com/uploads/Article/A100633/42fdbddb8a2e018b08d7456a8d069197.ris [bib] => https://www.explorationpub.com/uploads/Article/A100633/0891248ef548ad00b61b66e5883e15d8.bib [ens] => [Cited] => 2 [Cited_Time] => 2024-04-27 [CitethisArticle] => Sengupta P, Das R, Majumder P, Mukhopadhyay D. Connecting the ends: signaling via receptor tyrosine kinases and cytoskeletal degradation in neurodegeneration. Explor Neurosci. 2024;3:1–26. https://doi.org/10.37349/en.2024.00033 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-02-27 03:08:46 [Bib_Time] => 2024-02-27 03:08:46 [KeysWordContens] => Connecting the ends: signaling via receptor tyrosine kinases and cytoskeletal degradation in neurodegeneration, Receptor tyrosine kinase signaling, nuclear translocation, cytoskeletal remodeling, crosstalk, Rho GTPases, neurodegeneration, Rho/Rac/Cdc42, Receptor tyrosine kinases (RTKs) are known to perform versatile roles in disease landscapes, which determine the fate of the cell. Although much has been discussed from the perspective of proliferation, this review focuses on the impact of RTK-mediated signaling and its role in cytoskeletal degradation, the penultimate stage of cellular degeneration. In the case of degenerative diseases such as Alzheimer’s disease (AD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD), age-related macular degeneration (AMD), and type 2 diabetes mellitus (T2DM), RTK signaling has been reported to be perturbed in several studies. The implications of downstream signaling via these receptors through canonical and noncanonical pathways alter the status of actin filaments that provide structural integrity to cells. Degenerative signaling leads to the altered status of rat sarcoma (Ras), Ras homologous (Rho), Ras-related C3 botulinum toxin substrate (Rac), and cell division control protein 42 (Cdc42), the best-characterized components of the cytoskeleton remodeling machinery. RTKs, along with their diverse adaptor partners and other membrane receptors, affect the functionality of Rho family guanosine triphosphate hydrolases (GTPases), which are discussed in this review. To conclude, this review focuses on therapeutic strategies targeting RTKs and Rho GTPase-mediated pathways that can be more effective due to their combined multifactorial impact on neurodegenerative cascades. ,Priyanka Sengupta ... Debashis Mukhopadhyay [PublishedText] => Published [IsEdit] => 0 [AccountId] => 77 [Zh] => 1 ) [33] => Array ( [ArticleId] => 1104 [Create_Time] => 2024-02-21 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240221012208.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100634/100634.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100634/100634.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100634/100634_cover.png [JournalsId] => 8 [Title] => A mechanism for tuning proprioception proposed by research in Drosophila and mammals [Abstract] => Proprioception provides important sensory feedback regarding the position of an animal’s body and limbs in space. This interacts with a central pattern generator responsible for rhythmic movement, [AbstractComplete] =>Proprioception provides important sensory feedback regarding the position of an animal’s body and limbs in space. This interacts with a central pattern generator responsible for rhythmic movement, to adapt locomotion to the demands that an animal’s environment places on it. The mechanisms by which this feedback is enabled are poorly understood, which belies its importance: dysfunctional proprioception is associated with movement disorder and improving it can help reduce the severity of symptoms. Similarly, proprioception is important for guiding accurate robotic movement and for understanding how sensory systems capture and process information to guide action selection. It is therefore important to interpret research that investigates mechanisms of proprioception, to ask: what type of information do proprioceptive sensors capture, and how do they capture it? Work in mammalian models has made important progress towards answering this question. So too, has research conducted Drosophila. Fruit fly proprioceptors are more accessible than mammalian equivalents and can be manipulated using a unique genetic toolkit, so experiments conducted in the invertebrate can make a significant contribution to overall understanding. It can be difficult, however, to relate work conducted in different models, to draw general conclusions about proprioception. This review, therefore, explores what research in the fruit fly has revealed about proprioceptor function, to highlight its potential translation to mammals. Specifically, the present text presents evidence that differential expression of mechanoelectrical transducers contributes to tuning of fly proprioceptors and suggests that the same mechanism may play a role in tuning mammalian proprioceptors.
[Names] => Iain Hunter [Doi] => 10.37349/en.2024.00034 [Published] => February 21, 2024 [Viewed] => 405 [Downloaded] => 15 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2024.00034 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 0 [TitleAbbr] => Explor Neurosci. [Pages] => 2024;3:27–38 [Recommend] => 0 [Keywords] => Proprioception, mechanosensation, spindles, chordotonal neurons, Drosophila [DetailTitle] => [DetailUrl] => [Id] => 100634 [ris] => https://www.explorationpub.com/uploads/Article/A100634/206218ba3f0948572efbabff3680bcb9.ris [bib] => https://www.explorationpub.com/uploads/Article/A100634/c45be4852632503b11c42bdd2b443b15.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Hunter I. A mechanism for tuning proprioception proposed by research in Drosophila and mammals. Explor Neurosci. 2024;3:27–38. https://doi.org/10.37349/en.2024.00034 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-02-04 05:55:59 [Bib_Time] => 2024-02-04 05:55:59 [KeysWordContens] => A mechanism for tuning proprioception proposed by research in Drosophila and mammals, Proprioception, mechanosensation, spindles, chordotonal neurons, Drosophila , Proprioception provides important sensory feedback regarding the position of an animal’s body and limbs in space. This interacts with a central pattern generator responsible for rhythmic movement, to adapt locomotion to the demands that an animal’s environment places on it. The mechanisms by which this feedback is enabled are poorly understood, which belies its importance: dysfunctional proprioception is associated with movement disorder and improving it can help reduce the severity of symptoms. Similarly, proprioception is important for guiding accurate robotic movement and for understanding how sensory systems capture and process information to guide action selection. It is therefore important to interpret research that investigates mechanisms of proprioception, to ask: what type of information do proprioceptive sensors capture, and how do they capture it? Work in mammalian models has made important progress towards answering this question. So too, has research conducted Drosophila. Fruit fly proprioceptors are more accessible than mammalian equivalents and can be manipulated using a unique genetic toolkit, so experiments conducted in the invertebrate can make a significant contribution to overall understanding. It can be difficult, however, to relate work conducted in different models, to draw general conclusions about proprioception. This review, therefore, explores what research in the fruit fly has revealed about proprioceptor function, to highlight its potential translation to mammals. Specifically, the present text presents evidence that differential expression of mechanoelectrical transducers contributes to tuning of fly proprioceptors and suggests that the same mechanism may play a role in tuning mammalian proprioceptors. ,Iain Hunter [PublishedText] => Published [IsEdit] => 0 [AccountId] => 88 [Zh] => 1 ) [34] => Array ( [ArticleId] => 1107 [Create_Time] => 2024-02-22 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240222085017.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100635/100635.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100635/100635.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100635/100635_cover.png [JournalsId] => 8 [Title] => Antinociceptive effect and anti-inflammatory activity of 1,4-naphthoquinones in mice [Abstract] => Aim: The ability of synthetic 1,4-naphthoquinones (1,4-NQs) to prevent adenosine triphosphate (ATP)-induced and purinergic P2X7 receptor (P2X7R) mediated inflammation in macrophage and neurodegen [AbstractComplete] =>The ability of synthetic 1,4-naphthoquinones (1,4-NQs) to prevent adenosine triphosphate (ATP)-induced and purinergic P2X7 receptor (P2X7R) mediated inflammation in macrophage and neurodegeneration of neuronal cells in vitro was previously established. The aim of the present study was to investigate analgesic-like and anti-inflammatory activity of 1,4-NQs thioglucoside derivatives, compounds U-286 and U-548, in in vivo experiments.
Spectrofluorimetry approach and YO-PRO-1 fluorescent dye uptake determination were applied to study the effect of 1,4-NQs upon ATP-induced P2X7R mediated macropore formation in mouse neuroblastoma Neuro-2a cells and macrophages RAW 264.7 cells. An acetic acid-induced writhing test, hot plate test, and carrageenan-induced paw edema test were used as an in vivo mouse models to study the ability of 1,4-NQs to inhibit pain and inflammation. In the in vivo experiments, compounds were administered to mice intraperitoneally at dosages of 0.1 mg/kg, 1.0 mg/kg and 10.0 mg/kg. A group of animals that received injections of sterile water was used as a control. Each dosage group and the control group consisted of 6 mice.
In the present work the analgesic-like and anti-inflammatory activity of 1,4-NQs, U-286 and U-548, was demonstrated. Compound U-548 showed a significant inhibitory effect in antinociceptive tests reducing the number of mouse writhings and eliminating the latent time of mouse hind paw licking, correspondingly. Selected compounds were able to almost completely reduce the size of carrageenan-induced paw edema 24 h after injection and had a potent anti-inflammatory activity. Observed effects were accompanied with aptitude of studied 1,4-NQs to inhibit the formation of purinergic P2X7R macropore associated with inflammation and nociceptive pain.
The results obtained allow to consider compounds U-286 and U-548 and as a pharmacological basis for the development of new analgesic-like and anti-inflammatory drugs.
The ubiquity of circadian rhythms in living organisms has generally been accepted by researchers over the last century. Indeed, morphology and molecular biology of the circadian clock were described during the last fifty years. This main biological clock is located in the suprachiasmatic nucleus of the hypothalamus. This nucleus is connected with the retina by the retinohypothalamic tract. This way, light regulates the functioning of the biological clock and biological rhythms such as the sleep-wake cycle and other cyclic functions by releasing melatonin from the pineal body (PB) into the general circulation. Melatonin reaches the retina via the bloodstream as humoral feedback. More than a hundred years ago a reverse neuronal connection between the central nervous system and the retina was hypothesized. This so-called centrifugal visual or retinopetal system has been explored in detail in birds, but less information is available in mammals. In this work, the morphology and physiology of mammalian centrifugal visual pathways are reviewed. It is generally accepted that the centrifugal (retinopetal) fibers terminate mainly on the amacrine cells of the retina. Histaminergic fibers terminate on dopaminergic amacrine cells. Serotoninergic synapses were identified on ganglion cells. In addition, serotoninergic fibers were also associated with photoreceptor terminals. Luteinizing hormone releasing hormone fibers have been observed in birds, but not in mammalian retinas. In summary, based on the data available in the literature, it seems that the retinopetal system has a mandatory role in lower vertebrates, but a modulatory role in mammals. There is currently no adequate way to eliminate the centrifugal visual system that would better explain its true function.
[Names] => Viktória Vereczki ... Ágnes Csáki [Doi] => 10.37349/en.2024.00036 [Published] => February 22, 2024 [Viewed] => 442 [Downloaded] => 12 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/en.2024.00036 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 82 [TitleAbbr] => Explor Neurosci. [Pages] => 2024;3:51–64 [Recommend] => 0 [Keywords] => Rat, hamster, pineal body, virus labeling, electron microscopy, immunostaining, double labeling [DetailTitle] => Circadian Rhythm and Melatonin [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/82 [Id] => 100636 [ris] => https://www.explorationpub.com/uploads/Article/A100636/414626a298114e331a8fd3ed2a61d1a0.ris [bib] => https://www.explorationpub.com/uploads/Article/A100636/b12e1f8a2f3c84efb73d3bb8e71e5e6a.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Vereczki V, Köves K, Csáki Á. Current state of knowledge on the centrifugal visual system (including the pinealo-to-retinal connection) in mammals and its hypothesized role in circadian rhythms. Explor Neurosci. 2024;3:51–64. https://doi.org/10.37349/en.2024.00036 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-02-22 08:05:13 [Bib_Time] => 2024-02-07 01:41:13 [KeysWordContens] => Current state of knowledge on the centrifugal visual system (including the pinealo-to-retinal connection) in mammals and its hypothesized role in circadian rhythms, Rat, hamster, pineal body, virus labeling, electron microscopy, immunostaining, double labeling, The ubiquity of circadian rhythms in living organisms has generally been accepted by researchers over the last century. Indeed, morphology and molecular biology of the circadian clock were described during the last fifty years. This main biological clock is located in the suprachiasmatic nucleus of the hypothalamus. This nucleus is connected with the retina by the retinohypothalamic tract. This way, light regulates the functioning of the biological clock and biological rhythms such as the sleep-wake cycle and other cyclic functions by releasing melatonin from the pineal body (PB) into the general circulation. Melatonin reaches the retina via the bloodstream as humoral feedback. More than a hundred years ago a reverse neuronal connection between the central nervous system and the retina was hypothesized. This so-called centrifugal visual or retinopetal system has been explored in detail in birds, but less information is available in mammals. In this work, the morphology and physiology of mammalian centrifugal visual pathways are reviewed. It is generally accepted that the centrifugal (retinopetal) fibers terminate mainly on the amacrine cells of the retina. Histaminergic fibers terminate on dopaminergic amacrine cells. Serotoninergic synapses were identified on ganglion cells. In addition, serotoninergic fibers were also associated with photoreceptor terminals. Luteinizing hormone releasing hormone fibers have been observed in birds, but not in mammalian retinas. In summary, based on the data available in the literature, it seems that the retinopetal system has a mandatory role in lower vertebrates, but a modulatory role in mammals. There is currently no adequate way to eliminate the centrifugal visual system that would better explain its true function. ,Viktória Vereczki ... Ágnes Csáki [PublishedText] => Published [IsEdit] => 0 [AccountId] => 88 [Zh] => 1 ) [36] => Array ( [ArticleId] => 1129 [Create_Time] => 2024-02-26 [zipUrl] => https://www.explorationpub.com/uploads/zip/202402/20240226084030.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100637/100637.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100637/100637.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100637/100637_cover.png [JournalsId] => 8 [Title] => Cuban policosanol: a natural compound for ischemic stroke treatment [Abstract] => Stroke is among the leading causes of mortality and disability; therefore, it constitutes a relevant health problem. Cuban policosanol presents lipid-lowering, antiplatelet, antioxidant and vascular [AbstractComplete] =>Stroke is among the leading causes of mortality and disability; therefore, it constitutes a relevant health problem. Cuban policosanol presents lipid-lowering, antiplatelet, antioxidant and vascular endothelium protective properties, all of which give it a comprehensive anti-atherosclerotic effect. This review is aimed to show, analyze and discuss the main preclinical and clinical evidence of the effects of Cuban policosanol on ischemic stroke. Preclinical studies evidenced the anti-ischemic effects of preventive and therapeutic oral treatment with Cuban policosanol in Mongolian gerbils with cerebral ischemia induced by unilateral and permanent ligation of a carotid artery, and in global cerebral ischemia induced by bilateral clamping and recirculation of both carotids; being similar or superior to other anti-ischemic agents. Also, combination therapy with aspirin produced greater anti-stroke efficacy compared with aspirin monotherapy, but being similar to policosanol plus atorvastatin combination. This anti-stroke effect was associated to a serum thromboxane A2 (TxA2) concentrations reduction and prostacyclin (PgI2) increase, leading to a favorable TxA2/PgI2 balance, and also to the malondialdehyde (MDA) and sulfhydryl groups (SHG, lipid peroxidation and protein oxidation markers, respectively) reduction. Cuban policosanol combined with aspirin (standard therapy) improved and benefited patients with prior ischemic stroke in terms of functional and neurological outcomes, in open-label studies and in randomized, double-blind, controlled studies. These beneficial effects on stroke patients were associated with antioxidant and antiplatelet effects of policosanol. Also, the combinations of Cuban policosanol plus aspirin and atorvastatin plus aspirin compared in a clinical study significantly and similarly improved the neurological recovery of patients with ischemic stroke. Cuban policosanol was safe and well tolerated, with no serious adverse events occurring during the trials. In conclusion, Cuban policosanol is a safe and effective natural drug for ischemic stroke treatment, which is supported by preclinical and clinical evidences.
[Names] => Vivian Molina Cuevas, Ambar Oyarzábal Yera [Doi] => 10.37349/en.2024.00037 [Published] => February 26, 2024 [Viewed] => 389 [Downloaded] => 14 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2024.00037 [Inline] => 1 [Type] => 1 [Issue] => 1 [Topic] => 90 [TitleAbbr] => Explor Neurosci. [Pages] => 2024;3:65–79 [Recommend] => 0 [Keywords] => Cuban policosanol, ischemic stroke, preclinical, clinical evidence [DetailTitle] => Cerebral Ischemia, Genetics, Comorbidities, Risk Factors and New Therapeutic Options for Neurorestoration [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/90 [Id] => 100637 [ris] => https://www.explorationpub.com/uploads/Article/A100637/1775d3d90ae7fbd7e8fa6126e381332f.ris [bib] => https://www.explorationpub.com/uploads/Article/A100637/fbee7e8021397f566fc7a80319c59359.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Molina Cuevas V, Oyarzábal Yera A. Cuban policosanol: a natural compound for ischemic stroke treatment. Explor Neurosci. 2024;3:65–79. https://doi.org/10.37349/en.2024.00037 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-02-26 03:49:51 [Bib_Time] => 2024-02-22 07:36:47 [KeysWordContens] => Cuban policosanol: a natural compound for ischemic stroke treatment, Cuban policosanol, ischemic stroke, preclinical, clinical evidence, Stroke is among the leading causes of mortality and disability; therefore, it constitutes a relevant health problem. Cuban policosanol presents lipid-lowering, antiplatelet, antioxidant and vascular endothelium protective properties, all of which give it a comprehensive anti-atherosclerotic effect. This review is aimed to show, analyze and discuss the main preclinical and clinical evidence of the effects of Cuban policosanol on ischemic stroke. Preclinical studies evidenced the anti-ischemic effects of preventive and therapeutic oral treatment with Cuban policosanol in Mongolian gerbils with cerebral ischemia induced by unilateral and permanent ligation of a carotid artery, and in global cerebral ischemia induced by bilateral clamping and recirculation of both carotids; being similar or superior to other anti-ischemic agents. Also, combination therapy with aspirin produced greater anti-stroke efficacy compared with aspirin monotherapy, but being similar to policosanol plus atorvastatin combination. This anti-stroke effect was associated to a serum thromboxane A2 (TxA2) concentrations reduction and prostacyclin (PgI2) increase, leading to a favorable TxA2/PgI2 balance, and also to the malondialdehyde (MDA) and sulfhydryl groups (SHG, lipid peroxidation and protein oxidation markers, respectively) reduction. Cuban policosanol combined with aspirin (standard therapy) improved and benefited patients with prior ischemic stroke in terms of functional and neurological outcomes, in open-label studies and in randomized, double-blind, controlled studies. These beneficial effects on stroke patients were associated with antioxidant and antiplatelet effects of policosanol. Also, the combinations of Cuban policosanol plus aspirin and atorvastatin plus aspirin compared in a clinical study significantly and similarly improved the neurological recovery of patients with ischemic stroke. Cuban policosanol was safe and well tolerated, with no serious adverse events occurring during the trials. In conclusion, Cuban policosanol is a safe and effective natural drug for ischemic stroke treatment, which is supported by preclinical and clinical evidences. ,Vivian Molina Cuevas, Ambar Oyarzábal Yera [PublishedText] => Published [IsEdit] => 0 [AccountId] => 88 [Zh] => 1 ) [37] => Array ( [ArticleId] => 1181 [Create_Time] => 2024-04-07 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240407034034.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100638/100638.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100638/100638.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100638/100638_Cover.png [JournalsId] => 8 [Title] => Crop and pesticide effects on gut microbiota and neurological functions: a review [Abstract] => Pesticides are used to ensure the mass production and quality of foods, depending on the environment where they are grown. Trace amounts of pesticides are ingested through diet and high ratios of it [AbstractComplete] =>Pesticides are used to ensure the mass production and quality of foods, depending on the environment where they are grown. Trace amounts of pesticides are ingested through diet and high ratios of its components have been detected in humans. Neonicotinoid insecticides are nicotine analogs that disrupt neurons, induce neural excitation, and cause behavioral abnormalities and chronic toxicity. The herbicide glyphosate causes behavioral disorders due to abnormalities in the balance of intestinal microflora. These abnormalities can be found in the F2-generation and beyond. Glyphosate decreases the number and size of experimental animal fetuses, possibly through abnormal deoxyribonucleic acid methylation in parental germ cells, resulting in transgenerational toxicity. It also causes the death of dopamine neurons, which are believed to be involved in the development of Parkinson’s disease (PD). The intestinal microflora is considerably altered by ingesting pesticides used in crops. Lactic acid bacteria and some other intestinal bacteria have gut-regulating and immunomodulatory effects that have recently been implicated in neurological disorders, such as depression and dementia. Therefore, a healthy diet should be traced back to crops. An agriculture-medicine partnership linking “agriculture” and “preventive medicine” has recently been considered important based on the hypothesis that agriculture and health sectors should collaborate to create a healthy environment for producing healthy food. Although food considerations tend to focus on the functionality of vegetable and fruit components, that of environmental bacteria should also be considered.
[Names] => Tomomi Komura ... Yoshikazu Nishikawa [Doi] => 10.37349/en.2024.00038 [Published] => April 07, 2024 [Viewed] => 170 [Downloaded] => 12 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2024.00038 [Inline] => 1 [Type] => 0 [Issue] => [Topic] => 0 [TitleAbbr] => Explor Neurosci. [Pages] => 2024;3:80–102 [Recommend] => 0 [Keywords] => Crop, pesticide, neonicotinoid, glyphosate, epigenetics, intestinal microflora [DetailTitle] => [DetailUrl] => [Id] => 100638 [ris] => https://www.explorationpub.com/uploads/Article/A100638/fdb5c0e84d4c417cf1774341513dbf79.ris [bib] => https://www.explorationpub.com/uploads/Article/A100638/56dfce81bcd5f2f4e7179c3f4c8787a9.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Komura T, Yoshida M, Nishikawa Y. Crop and pesticide effects on gut microbiota and neurological functions: a review. Explor Neurosci. 2024;3:80–102. https://doi.org/10.37349/en.2024.00038 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-03-18 06:04:44 [Bib_Time] => 2024-03-18 06:04:44 [KeysWordContens] => Crop and pesticide effects on gut microbiota and neurological functions: a review, Crop, pesticide, neonicotinoid, glyphosate, epigenetics, intestinal microflora, Pesticides are used to ensure the mass production and quality of foods, depending on the environment where they are grown. Trace amounts of pesticides are ingested through diet and high ratios of its components have been detected in humans. Neonicotinoid insecticides are nicotine analogs that disrupt neurons, induce neural excitation, and cause behavioral abnormalities and chronic toxicity. The herbicide glyphosate causes behavioral disorders due to abnormalities in the balance of intestinal microflora. These abnormalities can be found in the F2-generation and beyond. Glyphosate decreases the number and size of experimental animal fetuses, possibly through abnormal deoxyribonucleic acid methylation in parental germ cells, resulting in transgenerational toxicity. It also causes the death of dopamine neurons, which are believed to be involved in the development of Parkinson’s disease (PD). The intestinal microflora is considerably altered by ingesting pesticides used in crops. Lactic acid bacteria and some other intestinal bacteria have gut-regulating and immunomodulatory effects that have recently been implicated in neurological disorders, such as depression and dementia. Therefore, a healthy diet should be traced back to crops. An agriculture-medicine partnership linking “agriculture” and “preventive medicine” has recently been considered important based on the hypothesis that agriculture and health sectors should collaborate to create a healthy environment for producing healthy food. Although food considerations tend to focus on the functionality of vegetable and fruit components, that of environmental bacteria should also be considered. ,Tomomi Komura ... Yoshikazu Nishikawa [PublishedText] => Published [IsEdit] => 0 [AccountId] => 55 [Zh] => 1 ) [38] => Array ( [ArticleId] => 1199 [Create_Time] => 2024-04-08 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240408021928.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100639/100639.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100639/100639.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100639/100639_cover.png [JournalsId] => 8 [Title] => Role of antioxidants as immunity booster in obesity and diabetes: a systematic review on neuro-gliopathies perspective [Abstract] => Background: The main objective of the study was to carry out a systematic literature review to investigate the beneficial role of antioxidants in obesity and diabetes and the association of antio [AbstractComplete] =>The main objective of the study was to carry out a systematic literature review to investigate the beneficial role of antioxidants in obesity and diabetes and the association of antioxidants in neuro-gliopathies and gut microbiome on antioxidant production and enteric nervous system (ENS) protection.
A literature search was done electronically on 8 June 2022 in the databases Google Scholar, and PubMed, reviewing all the articles published in English. There were no limitations for the study (region, or any time frame). The study included randomized controlled trials (RCTs) and observational studies on a human subject, primarily focusing on information such as a change in body weight, body mass index (BMI), waist-to-height ratio (WHtR), waist-to-hip ratio (WHR), fasting blood glucose level, glycated haemoglobin (HbA1c), and other parameters that connected with diabetes and obesity. The search was also conducted for neuro-gliopathies and gut microbiome.
The beginning database search picked out a total of 2,428 articles, 1,310 in PubMed, 876 in Google Scholar, and 242 records from other sources. A total of 2,040 (total duplicates 388) was found after removing the duplicated articles, and after reading the title and abstracts were further decreased to 139 full-text articles. These 139 studies went for full-text analysis, which resulted in the exclusion of 123 studies and generated a final 16 articles included for systemic analysis.
This literature search of present studies shows the interconnection between antioxidant intake among obese and diabetes neuro-gliopathies. The findings indicate both obese and diabetic patients have a minimum content of antioxidants, especially carotenoids, retinol, ascorbic acid, tocopherol, magnesium, and zinc. While few research illustrated that ingestion of the abovementioned antioxidants was lowered among diabetes and obese subjects in contrast with their normal-weight population, this was not endorsed by every study.
Brain metastasis is the most prevalent neurologic problem of systemic cancer and it can increase the mortality rate in patients with cancer. It occurs more in patients with lung cancer, breast cancer, and melanoma. There are several molecular mechanisms in cancer cell progression, invasion, and location in new places during brain metastasis. Significant interactions between cancer cells, the brain microenvironment, and the blood-brain barrier (BBB) play a major role in brain metastasis. This study will focus on molecular mechanisms that contribute to cancer metastasis into the brain and finding new treatments with molecular research. Treatment strategies in patients with brain metastasis include surgical resection, radiotherapy, and chemotherapy; however, the penetration of chemotherapy drugs beyond the BBB is limited. Studying molecular, cellular, and physical mechanisms in brain metastasis helps to improve new strategies in drug delivery across the BBB. There are significant impacts of ion channels in brain metastasis and cancer treatment failure. Targeting molecular mechanisms and ion channels in brain metastasis led to increasing the better response in these patients. In this way, nano-drugs have caused a revolution in effective targeting and drug delivery in cancer treatment. This review describes the advances to facilitate the penetration of drugs in the BBB by using nano-drugs especially those that are targeting ion channels.
[Names] => Zohreh Khosravi Dehaghi [Doi] => 10.37349/en.2024.00040 [Published] => April 10, 2024 [Viewed] => 196 [Downloaded] => 8 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2024.00040 [Inline] => 1 [Type] => 0 [Issue] => 0 [Topic] => 328 [TitleAbbr] => Explor Neurosci. [Pages] => 2024;3:130–143 [Recommend] => 0 [Keywords] => Brain metastases, genetic alterations, blood-brain barrier, epithelial-mesenchymal transition, ion channel, nano-drug [DetailTitle] => Current Approaches to Malignant Tumors of the Nervous System [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/328 [Id] => 100640 [ris] => https://www.explorationpub.com/uploads/Article/A100640/4cba28590f75aa21a79bd0bc8da04b2c.ris [bib] => https://www.explorationpub.com/uploads/Article/A100640/21ec5a88536a61706a6524b1741c9b44.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Dehaghi ZK. Brain metastasis from the perspective of molecular mechanisms and treatment, presenting a new approach for targeting ion channels by nano drugs. Explor Neurosci. 2024;3:130–43. https://doi.org/10.37349/en.2024.00040 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-04-09 03:53:10 [Bib_Time] => 2024-04-09 03:53:10 [KeysWordContens] => Brain metastasis from the perspective of molecular mechanisms and treatment, presenting a new approach for targeting ion channels by nano drugs, Brain metastases, genetic alterations, blood-brain barrier, epithelial-mesenchymal transition, ion channel, nano-drug, Brain metastasis is the most prevalent neurologic problem of systemic cancer and it can increase the mortality rate in patients with cancer. It occurs more in patients with lung cancer, breast cancer, and melanoma. There are several molecular mechanisms in cancer cell progression, invasion, and location in new places during brain metastasis. Significant interactions between cancer cells, the brain microenvironment, and the blood-brain barrier (BBB) play a major role in brain metastasis. This study will focus on molecular mechanisms that contribute to cancer metastasis into the brain and finding new treatments with molecular research. Treatment strategies in patients with brain metastasis include surgical resection, radiotherapy, and chemotherapy; however, the penetration of chemotherapy drugs beyond the BBB is limited. Studying molecular, cellular, and physical mechanisms in brain metastasis helps to improve new strategies in drug delivery across the BBB. There are significant impacts of ion channels in brain metastasis and cancer treatment failure. Targeting molecular mechanisms and ion channels in brain metastasis led to increasing the better response in these patients. In this way, nano-drugs have caused a revolution in effective targeting and drug delivery in cancer treatment. This review describes the advances to facilitate the penetration of drugs in the BBB by using nano-drugs especially those that are targeting ion channels. ,Zohreh Khosravi Dehaghi [PublishedText] => Published [IsEdit] => 0 [AccountId] => 88 [Zh] => 1 ) [40] => Array ( [ArticleId] => 1225 [Create_Time] => 2024-04-12 [zipUrl] => https://www.explorationpub.com/uploads/zip/202404/20240412062931.zip [xmlUrl] => https://www.explorationpub.com/uploads/Article/A100641/100641.xml [pdfUrl] => https://www.explorationpub.com/uploads/Article/A100641/100641.pdf [coverUrl] => https://www.explorationpub.com/uploads/Article/A100641/100641_cover.png [JournalsId] => 8 [Title] => First outcomes of a therapeutic platform for drug resistant epilepsy based on transcutaneous electrical vagus nerve stimulation [Abstract] => Aim: The aim of this paper is to discuss the main features and first outcomes of a therapeutic platform proposed to implement a public health therapeutic service for patients suffering refractory [AbstractComplete] =>The aim of this paper is to discuss the main features and first outcomes of a therapeutic platform proposed to implement a public health therapeutic service for patients suffering refractory epilepsy.
The proposal is a three-layer system composed by a new portable therapy device and two software applications. The therapy is transcutaneous electrical vagus nerve stimulation, known as tVNS. The primary layer is composed of tVNS devices, configured for each patient according to the instructions provided by the specialists. The middle layer is named “hospital data collector” (HDC), its main tasks are the patient enrollment, the device setup, and the database maintenance to store therapeutic parameters and session events together with the information cited previously. Each hospital center runs a HDC that is connected to a cloud application named “system cloud application (SCA)” which concentrates all the data supplied by the HDCs. Artificial intelligence methods are integrated in the SCA to predict the treatment effectiveness for every new patient based on the accumulated knowledge from the enrolled previously.
A version of the proposed system is running at the Institute of Neurology and Neurosurgery. The sensitivity of the therapeutic device with the proposed treatment protocol reaches 83.33% in the 18-patient pilot trial carried out.
The proposed approach seems a useful therapeutic tool based on the pilot trial outcomes. The developed device is comfortable and suitable for the intended use. The proposed system has created the essential conditions to feed and grow a knowledge, a basic element to predict the treatment effectiveness for each new patient. It is a promising option for a refractory epilepsy therapy service.
Major depressive disorder (MDD) is a common mental disorder associated with significant suffering and disability. Recent evidence has highlighted the role of the gut-brain axis in the pathogenesis of MDD. Enteric glial cells are a structurally and functionally diverse population that plays a key role in regulating enteric nervous function and maintaining intestinal mucosal integrity. These cells may be implicated in the origin of several digestive and extra-digestive disorders, known as enteric neuro-gliopathies (ENG). This paper reviews the evidence that MDD may also belong to the category of ENG. Animal models suggest that environmental adversity can lead to enteric glial dysfunction and depressive-like behaviors. Conditions that are highly comorbid with MDD, both intestinal and extra-intestinal, have been linked to enteric glial alterations. Peripheral blood markers linked to glial integrity and function are altered in patients with MDD, and certain treatments for MDD may have beneficial effects on enteric glial functioning. Though much of this evidence is indirect and provisional, it suggests that MDD may belong to the group of ENG. Further investigation of enteric glial functioning in MDD may yield valuable insights into the pathophysiology and treatment of this disorder.
[Names] => Ravi Philip Rajkumar [Doi] => 10.37349/en.2024.00042 [Published] => April 30, 2024 [Viewed] => 10 [Downloaded] => 2 [Subject] => Review [Year] => 2024 [CiteUrl] => https://api.crossref.org/works/10.37349/en.2024.00042 [Inline] => 0 [Type] => 0 [Issue] => [Topic] => 273 [TitleAbbr] => Explor Neurosci. [Pages] => 2024;3:156–174 [Recommend] => 0 [Keywords] => Major depression, gut-brain axis, gut microbiota, inflammation, stress, enteric glial cells, enteric neuro-gliopathy [DetailTitle] => Enteric Neuro-Gliopathies: Ready for Prime Time? [DetailUrl] => https://www.explorationpub.com/Journals/en/Special_Issues/273 [Id] => 100642 [ris] => https://www.explorationpub.com/uploads/Article/A100642/18aafaeae32b6f84d55dedd09e5220fb.ris [bib] => https://www.explorationpub.com/uploads/Article/A100642/aef7863d8fe24816eb044597c03e83f4.bib [ens] => [Cited] => 0 [Cited_Time] => [CitethisArticle] => Rajkumar RP. Do enteric glial cells play a role in the pathophysiology of major depression? Explor Neurosci. 2024;3:156–74. https://doi.org/10.37349/en.2024.00042 [Jindex] => 0 [CName] => [CEmail] => [Ris_Time] => 2024-04-26 01:12:08 [Bib_Time] => 2024-04-26 01:12:08 [KeysWordContens] => Do enteric glial cells play a role in the pathophysiology of major depression?, Major depression, gut-brain axis, gut microbiota, inflammation, stress, enteric glial cells, enteric neuro-gliopathy, Major depressive disorder (MDD) is a common mental disorder associated with significant suffering and disability. Recent evidence has highlighted the role of the gut-brain axis in the pathogenesis of MDD. Enteric glial cells are a structurally and functionally diverse population that plays a key role in regulating enteric nervous function and maintaining intestinal mucosal integrity. These cells may be implicated in the origin of several digestive and extra-digestive disorders, known as enteric neuro-gliopathies (ENG). This paper reviews the evidence that MDD may also belong to the category of ENG. Animal models suggest that environmental adversity can lead to enteric glial dysfunction and depressive-like behaviors. Conditions that are highly comorbid with MDD, both intestinal and extra-intestinal, have been linked to enteric glial alterations. Peripheral blood markers linked to glial integrity and function are altered in patients with MDD, and certain treatments for MDD may have beneficial effects on enteric glial functioning. Though much of this evidence is indirect and provisional, it suggests that MDD may belong to the group of ENG. Further investigation of enteric glial functioning in MDD may yield valuable insights into the pathophysiology and treatment of this disorder. ,Ravi Philip Rajkumar [PublishedText] => Published [IsEdit] => 0 [AccountId] => 77 [Zh] => 0 ) )