There is a complex relationship between circadian rhythm dysfunctions and various psychiatric disorders. Circadian (~24 h) rhythms indicate the rhythmic change of different physiological activities in relation to the environmental light-dark cycle. Shift work, light exposure at night, and chronic and acute jet lag affect circadian rhythm that have a negative impact on psychological functions, and behaviors. Additionally, professional stress, mental instability, and social disintegration influence psychiatric disorders. PubMed/MEDLINE, Springer Nature, Science Direct (Elsevier), Wiley Online, ResearchGate, and Google Scholar databases were searched to collect relevant articles. Circadian rhythm disruption causes impaired neurotransmitter release, impaired melatonin and cortisol rhythm, metabolic dysfunctions, neuroinflammation, and neural apoptosis; collectively these factors influence the development of psychiatric disorders. Circadian dysfunction also alters the expression of several clock control genes in the mesolimbic areas that are associated with pathologies of psychiatric disorders. Additionally, chronotherapy and applications of anti-psychotic medicine can improve psychiatric diseases. This review focuses on the effects of circadian clock dysfunction on the vulnerability of psychiatric disorders and the implications of chronotherapy.

The PRECEDE-PROCEED model is a comprehensive planning and theoretical framework that incorporates epidemiological, environmental, behavioral, and social factors systematically to design, implement, and evaluate health promotion programs. As such, PRECEDE-PROCEED is a highly effective tool for addressing complex and significant public health concerns like postpartum depression (PPD). PPD negatively impacts mothers and their infants, with studies showing that approximately one in eight mothers experience PPD, leading to adverse effects on maternal functioning and infant development. However, access to specialized evidence-based treatment remains significantly limited due to barriers including social determinants of health. This paper explores the application of the PRECEDE-PROCEED model as a planning and theoretical framework for the design and development of MommaConnect, an innovative digital healthcare platform aimed at reducing PPD symptoms and improving maternal-infant interaction while overcoming barriers to treatment. Key components of the MommaConnect design and development process are mapped onto the steps of the PRECEDE-PROCEED model. MommaConnect features are aligned with specific stages of the model, from assessing, predisposing, enabling, and reinforcing factors to designing, implementing, and evaluating the intervention. By leveraging this model, MommaConnect represents a promising innovative approach to address PPD to improve maternal functioning and infant health in a digitally-enabled era. This paper underscores the importance of utilizing a framework like the PRECEDE-PROCEED model in the design and development of innovative healthcare solutions.

A short overview of the main features of progressive myoclonus epilepsies (PMEs), such as Lafora disease (LD), neuronal ceroid lipofuscinoses (NCLs), and myoclonus epilepsy with ragged-red fibers (MERRF) is given. The stress of this review paper is put on one of the PME’s, the Unverricht-Lundborg disease (ULD)—EPM1, which is caused by mutations in the human cystatin B gene (stefin B is an alternative protein’s name). However, different other genes/proteins were found mutated in patients presenting with EPM1-like symptoms. By understanding their function and pathophysiological roles, further insights into the underlying processes of EPM1 can be obtained. On a broader scale, common pathophysiological mechanisms exist between ULD, LD and NCLs, such as, reactive glia, synaptic remodeling, neuronal hyperexcitability, impairements in the lysosomal/endocytosis system, cytoskeletal functions, and mitochondria. Oxidative stress is also in common. By understanding the underlying molecular and cellular processes, early interventions, better therapies and eventually, by using modern stem cell, gene editing or replacement methods, a cure can be expected.

Depression is on the rise and medication does not always provide satisfactory relief. This raises the question of a treatment gap that has not yet been (sufficiently) addressed. Inflammation and oxidative stress play an important pathophysiological role, which also leads to a deficiency of antioxidants such as vitamin C. This perspective mini-review reflects the results of a PubMed search combining the search terms depression with inflammation, oxidative stress and vitamin C. Vitamin C is an important antioxidant and co-factor for many neuronal metabolic and epigenetic pathways, and a deficiency is associated with depression and cognitive disorders. Inadequate vitamin C blood levels that do not yet result in somatic symptoms may induce neuropsychiatric scurvy, which is associated with increased neuroinflammation and characterized by depression and cognitive impairment. Experimental studies show that vitamin C has multifactorial effects on metabolic pathways relevant to depression. Treatment of vitamin C deficiency, which is more common than appreciated, should be considered in the management of depressed patients. Further studies should investigate whether the pharmacological administration of vitamin C has additional effects beyond the correction of deficiency.

Depression poses a significant global health burden, yet current therapeutic approaches focusing on monoaminergic neurotransmission often fall short of achieving full remission and managing acute episodes effectively. This article explores novel treatment avenues beyond conventional monoaminergic approaches, focusing on emerging strategies targeting glutamatergic modulation, electrophysiological/magnetic brain stimulation techniques, anti-inflammatory agents, gut-brain axis interventions, gamma-aminobutyric acid (GABA) modulation, and psychedelic-assisted therapy. Through a narrative review of recent literature, this paper elucidates the mechanisms, clinical efficacy, safety profiles, and future directions of these innovative treatments. These insights offer valuable perspectives for advancing depression management and bridging existing therapeutic gaps.

Alzheimer’s disease (AD) is a major type of dementia and neurodegenerative disease, characterized by memory loss and cognitive decline. Over decades, significant efforts have been dedicated to finding its cause, pathogenic mechanisms, biomarkers for early detection, and clinical trials for its treatment. Earlier approved drugs mainly ameliorated the symptoms of AD, until recent years when two drugs targeting amyloid-beta (Aβ) protein were approved to slow down the progression of the disease. This review article encompasses the history of drug development in treating AD and clinical trials that failed and succeeded. Clinicaltrials.org website was systematically searched and screened for randomized controlled trials with results posted in the past 10 years. Among the 3,388 AD clinical trials, 211 interventional studies registered under AD have met eligibility. This review includes the interventional targets for drug discovery such as Aβ, tau, neurotransmitter receptors, neuroinflammation, multi-target studies, repurposing pharmacological agents, non-pharmacological interventions, and clinical therapy development for the neuropsychiatric symptoms of dementia. Current clinical trials are ongoing and no results are available as of yet. With the vast choices of drug targets that have been investigated, this review aims to present some insights into future AD drug design and trials and contribute to our ongoing efforts to find the cure.

Neurological disorders including neurodegenerative disorders continue to pose significant therapeutic challenges. Triterpenoids, a diverse group of natural compounds found abundantly in plants, possess promising neuroprotective properties. This review aims to explore the potential of triterpenoids in mitigating neurodegeneration through various mechanisms, including antioxidant, anti-inflammatory, and anti-apoptotic activities. The neuroprotective potential of some notable triterpenoids, such as asiatic acid, asiaticoside, madecassoside, bacoside A, bacopaside I, ganoderic acids, and lucidenic acids are discussed in terms of their ability to modulate key pathways implicated in neurological disorders. Additionally, the potential therapeutic applications of triterpenoids in Alzheimer’s disease, Parkinson’s disease, cerebral ischemia, spinal cord injury, and epilepsy are examined. Furthermore, the review also underlines the challenges for the development of triterpenoids as neuroprotective agents, including the need for further preclinical and clinical studies to elucidate their efficacy and safety for translation into clinical practice.