Scholarlink

<p>Post-stroke depression (PSD) is a common and clinically significant complication of stroke and is associated with decreased rehabilitation potential and an elevated risk of mortality. The prevalence of PSD ranges from 25 to 59% depending on the time of observation, peaking in the first years after stroke. The pathogenesis of PSD is the result of 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, decreased neuroplasticity (including BDNF deficiency), and disruption of the integrity of neural networks. The clinical picture is characterized by a set of affective (apathy, anhedonia), cognitive (impaired executive function), and insomnia disorders. Although selective serotonin reuptake inhibitors remain the first-line treatment for post-stroke depression, a modern therapeutic approach requires all stages of the pathogenesis to be addressed. A promising approach consists of the use of antidepressants with complex mechanisms of action, such as the original fluvoxamine, which combines a serotonergic effect with anti-inflammatory and neuroprotective properties due to sigma-1 receptor agonism. The treatment of PSD can be optimized by implementation of a personalized approach, including thorough screening and comprehensive correction of identified disorders.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Neuroinflammation as a Key Target in the Treatment of Post-Stroke Depression

  • 期刊论文

  • 发表日期：

    2026年7月27日

查看全文
  • T. B. Bender,
  • Yu. N. Bykov

摘要

Post-stroke depression (PSD) is a common and clinically significant complication of stroke and is associated with decreased rehabilitation potential and an elevated risk of mortality. The prevalence of PSD ranges from 25 to 59% depending on the time of observation, peaking in the first years after stroke. The pathogenesis of PSD is the result of 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, decreased neuroplasticity (including BDNF deficiency), and disruption of the integrity of neural networks. The clinical picture is characterized by a set of affective (apathy, anhedonia), cognitive (impaired executive function), and insomnia disorders. Although selective serotonin reuptake inhibitors remain the first-line treatment for post-stroke depression, a modern therapeutic approach requires all stages of the pathogenesis to be addressed. A promising approach consists of the use of antidepressants with complex mechanisms of action, such as the original fluvoxamine, which combines a serotonergic effect with anti-inflammatory and neuroprotective properties due to sigma-1 receptor agonism. The treatment of PSD can be optimized by implementation of a personalized approach, including thorough screening and comprehensive correction of identified disorders.