Chlorpromazine as a Potential Antipsychotic Choice in COVID-19 Treatment

Electroconvulsive therapy (ECT) remains one of the most effective interventions for treatment-resistant psychiatric disorders, particularly major depressive disorder and bipolar disorder. Despite extensive clinical and preclinical investigations, the precise neurobiological mechanisms underlying ECT’s therapeutic effects are not fully understood. This review explores the molecular and cellular pathways involved in ECT, emphasizing its impact on neurotrophic signaling, oxidative stress, apoptosis, and neuroplasticity. Evidence suggests that ECT modulates brain-derived neurotrophic factor and other neurotrophic factors, promoting synaptic plasticity and neuronal survival. Additionally, ECT influences the hypothalamic–pituitary–adrenal axis, reduces neuroinflammation, and alters neurotransmitter systems, contributing to its antidepressant effects. Recent findings also highlight the role of mitochondrial function and oxidative stress regulation in ECT-induced neural adaptation. By synthesizing current molecular insights, this review provides a comprehensive perspective on the neurobiological mechanisms of ECT, offering potential directions for future research and therapeutic advancements in brain stimulation.

Background: Insomnia is markedly more prevalent in rheumatoid arthritis (RA) patients than in the general population and is closely linked to pain, fatigue, psychological comorbidities, and systemic inflammation. Evidence suggests a bidirectional relationship, where active disease worsens sleep quality, while poor sleep amplifies inflammatory activity and symptom severity. Methods: A narrative review was conducted using PubMed, Scopus, Web of Science, and Embase to identify studies from the last 15 years involving adult RA patients. Inclusion criteria required assessment of insomnia or sleep quality in relation to disease activity, treatment outcomes, or inflammatory markers. Data from clinical trials, cohort studies, and reviews were synthesized to examine prevalence, mechanisms, and therapeutic implications. Results: Insomnia affects up to 45% of RA patients and correlates with higher DAS28 scores, elevated CRP/ESR, increased pain sensitivity, and reduced quality of life. Contributing factors include chronic pain, stiffness, elevated IL-6 and TNF-α, depression, anxiety, and medication side effects. Conventional DMARDs, corticosteroids, and biologics indirectly improve sleep via inflammation control, with IL-6 inhibition showing potential sleep-specific benefits. Psychotropic agents may help in comorbid depression/anxiety but are best combined with cognitive behavioral therapy for insomnia (CBT-I). Conclusions: Insomnia is a prevalent, multifactorial problem in RA that adversely affects disease activity, symptom burden, and functional outcomes. Integrating sleep evaluation into routine RA management and adopting interdisciplinary strategies that address both inflammation and sleep disturbance may enhance patient outcomes. High-quality longitudinal studies using objective sleep measures are needed to clarify causal relationships and optimize therapy.

Access full-text academic articles: J-STAGE is an online platform for Japanese academic journals.

Electroconvulsive therapy (ECT) remains one of the most effective interventions for treatment-resistant psychiatric disorders, particularly major depressive disorder and bipolar disorder. Despite extensive clinical and preclinical investigations the precise neurobiological mechanisms underlying ECT’s therapeutic effects are not fully understood. This review explores the molecular and cellular pathways involved in ECT, emphasizing its impact on neurotrophic signaling, oxidative stress, apoptosis, and neuroplasticity. Evidence suggests that ECT modulates brain-derived neurotrophic factor (BDNF) and other neurotrophic factors, promoting synaptic plasticity and neuronal survival. Additionally, ECT influences the hypothalamic-pituitary-adrenal (HPA) axis, reduces neuroinflammation, and alters neurotransmitter systems, contributing to its antidepressant effects. Recent findings also highlight the role of mitochondrial function and oxidative stress regulation in ECT-induced neural adaptation. By synthesizing current molecular insights, this review provides a comprehensive perspective on the neurobiological mechanisms of ECT, offering potential directions for future research and therapeutic advancements in brain stimulation.

Insomnia is the most prevalent sleep disorder worldwide, affecting up to 30% of the population, and is frequently accompanied by cognitive complaints and measurable cognitive impairments. Chronic insomnia is characterized by persistent hyperarousal across physiological, cognitive, and neurobiological domains, which may compromise multiple cognitive systems. This review synthesizes current evidence on the impact of insomnia on major cognitive domains, including attention, language, memory and learning, executive functions, perceptual–motor skills, and social cognition. We critically evaluate methodological factors contributing to heterogeneous findings across studies, such as variability in diagnostic criteria, insomnia phenotypes, cognitive assessments, and sample characteristics. Additionally, we summarize emerging evidence on neuroanatomical and molecular correlates of insomnia-related cognitive impairment, including alterations in hippocampal and prefrontal brain structures, amyloid-β accumulation, dysregulation of brain-derived neurotrophic factor, neurotransmitter imbalance, neuroinflammation, and disrupted signaling pathways. Insights from preclinical studies show mechanistic links between sleep loss, synaptic dysfunction, oxidative stress, and memory decline. Despite substantial advances, the precise pathophysiological mechanisms underlying cognitive dysfunction in insomnia remain incompletely understood, suggesting that cognitive impairment arises from the convergence of multiple biological processes rather than a single causal pathway. A deeper mechanistic understanding is essential for developing targeted interventions for preventing cognitive decline in individuals with insomnia.