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Post-stroke depression (PSD) is a common and clinically significant stroke complication associated with impaired rehabilitation potential and increased mortality risk. The prevalence of PSD varies from 25% to 59% depending on the duration of observation, reaching a peak in the first years after a stroke. The pathogenesis of PSD results from a complex interplay of biological and psychological factors that extends well beyond monoamine deficiency. Damage to monoaminergic pathways, neuroinflammation, hypothalamic-pituitary-adrenal axis dysfunction, decreased neuroplasticity (including BDNF deficiency), and impaired neural network integrity play a key role. The clinical presentation includes a complex of affective (apathy, anhedonia), cognitive (impaired executive functions), and dyssomnia disorders. While selective serotonin reuptake inhibitors remain the first choice for treatment of PSD, the current therapeutic approach requires targeting all pathogenesis links. A promising direction is the use of antidepressants with a complex mechanism of action, such as the original fluvoxamine, which combines serotonergic effects with anti-inflammatory and neuroprotective properties through sigma-1 receptor agonism. Optimizing PSD treatment is possible through a personalized approach that includes thorough screening and comprehensive correction of identified disorders. Show less

Substance Use Disorders (SUD) have escalated into a global public health crisis, with their core pathology encompassing not only physiological dependence and a heightened risk of relapse, but also profound social cognitive impairments caused by chronic substance abuse. These impairments constitute a major barrier to rehabilitation yet remain largely overlooked in current treatment frameworks. This review develops and substantiates an innovative theoretical framework centered on the "Exercise-Irisin-Social Brain" axis. We propose a core pathway hypothesis: regular exercise can induce the release of the myokine irisin from skeletal muscle, which then enters the bloodstream and crosses the blood-brain barrier to act on the prefrontal cortex, which is the central hub of social cognition and executive function. Through potential mechanisms including the upregulation of brain-derived neurotrophic factor and the suppression of neuroinflammation, irisin may contribute to the repair of the executive function network that underlies higher-order social cognition, thereby improving social cognitive abilities and ultimately providing a supportive foundation for the reconstruction of social functioning in individuals with SUD. This new paradigm not only provides a testable biological pathway for understanding how exercise may repair the addicted brain, but also transcends the limitations of traditional models that focus primarily on withdrawal and relapse, by elevating rehabilitation goals to emphasize the restoration of social functioning. Show less

ObjectiveTo evaluate the effects of a combined psychological and functional exercise intervention on emotion, quality of life, and brain-derived neurotrophic factor (BDNF) levels in patients with Parkinson's disease (PD).MethodsIn this randomized controlled trial, 172 patients with PD were randomly assigned into 2 groups with 86 patients in each group. The control group received routine care, while the intervention group received a 12-week intervention combining psychological support with functional exercise in addition to routine care. Hamilton Anxiety Scale (HAMA), Hamilton Depression Scale (HAMD), Parkinson's Disease Questionnaire-39 (PDQ-39), Barthel Index, Movement Disorder Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS), and serum BDNF levels were assessed before and after the intervention. Adherence rates were also determined for each group. Spearman correlation analysis was used to examine associations between changes in BDNF (ΔBDNF) and changes in HAMA (ΔHAMA) and HAMD (ΔHAMD) scores.ResultsAt the end of the 12-week clinical trial, the intervention group demonstrated significantly lower HAMA, HAMD, PDQ-39, and MDS-UPDRS scores ( Show less