[Neuroinflammation as a therapeutic target in post-stroke depression].
📄 Abstract
Post-stroke depression (PSD) is a common and clinically significant complication of stroke, associated with worse rehabilitation potential and increased mortality risk. The prevalence of PSD varies from 25% to 59%, depending on the duration of follow-up, peaking in the first years after the stroke event. The pathogenesis of PSD results from a complex interplay of biological and psychological factors, extending far beyond monoamine deficiency. Key roles are played by damage to monoaminergic pathways, neuroinflammation, dysfunction of the hypothalamic-pituitary-adrenal axis, reduced neuroplasticity (including BDNF deficit), and impaired integrity of neuronal networks. The clinical picture is characterized by a complex of affective (apathy, anhedonia), cognitive (executive dysfunction), and dyssomnic disorders. Although selective serotonin reuptake inhibitors remain the first-line treatment, the modern therapeutic approach to PSD requires targeting all components of its pathogenesis. A promising direction is the use of antidepressants with a multimodal mechanism of action, such as the original drug fluvoxamine, which combines serotonergic effects with anti-inflammatory and neuroprotective properties via sigma-1 (σ1) receptor agonism. Optimizing PSD treatment is achievable through the implementation of a personalized approach, including long-term screening and comprehensive management of the identified disorders.