Feng Xinyu, Ma Xiaojuan, Li Juan, Zhou Qing, Liu Yao, Song Jingyi, Liu Jiaqi, Situ Qingqing, Wang Lingyue, Zhang Jingzhi, Lin Facai
Aging Dis. 2024 Feb 9;16(1):209-38. doi: 10.14336/AD.2024.0203.
Post-stroke depression (PSD) is a complex mood disorder that emerges in individuals following a stroke, characterized by the development of depressive symptoms. The pathogensis of PSD is diverse, with inflammation playing a vital role in its onset and progression. Emerging evidence suggests that microglial activation, astrocyte responses, nuclear factor κB(NF-κB) signaling, dysregulation of the hypothalamic pituitary adrenal (HPA) axis, alterations in brain-derived neurotrophic factor (BDNF) expression, neurotransmitter imbalances, adenosine triphosphate (ATP) and its receptors and oxidative stress are intricately linked to the pathogenesis of PSD. The involvement of inflammatory cytokines in these processes highlights the significance of the inflammatory pathway. Integrating these hypotheses, the inflammatory mechanism offers a novel perspective to expand therapeutic strategies for PSD.
中风后抑郁症(PSD)是一种复杂的情绪障碍,出现在中风后的个体中,其特征是出现抑郁症状。PSD的发病机制多种多样,炎症在其发病和进展中起着至关重要的作用。新出现的证据表明,小胶质细胞激活、星形胶质细胞反应、核因子κB(NF-κB)信号传导、下丘脑-垂体-肾上腺(HPA)轴失调、脑源性神经营养因子(BDNF)表达改变、神经递质失衡、三磷酸腺苷(ATP)及其受体以及氧化应激与PSD的发病机制密切相关。炎症细胞因子在这些过程中的参与突出了炎症途径的重要性。综合这些假说,炎症机制为扩展PSD的治疗策略提供了一个新的视角。