Investigating the Potential Mechanisms and Therapeutic Targets of Inflammatory Cytokines in Post-stroke Depression

Post-stroke depression (PSD) affects approximately one-third of stroke survivors, severely impacting general recovery and quality of life. Despite extensive studies, the exact mechanisms underlying PSD remain elusive. However, emerging evidence implicates proinflammatory cytokines, including interleukin-1 & beta;, interleukin-6, tumor necrosis factor-alpha, and interleukin-18, play critical roles in PSD development. These cytokines contribute to PSD through various mechanisms, including hypothalamic-pituitary-adrenal (HPA) axis dysfunction, neurotransmitter alterations, neurotrophic factor changes, gut microbiota imbalances, and genetic predispositions. This review is aimed at exploring the role of cytokines in stroke and PSD while identifying their potential as specific therapeutic targets for managing PSD. A more profound understanding of the mechanisms regulating inflammatory cytokine expression and anti-inflammatory cytokines like interleukin-10 in PSD may facilitate the development of innovative interventions to improve outcomes for stroke survivors experiencing depression.

Automated summary

Post-stroke depression (PSD) is prevalent in about one-third of stroke survivors and has a severe impact on recovery and quality of life. The exact mechanisms of PSD are still unknown, but proinflammatory cytokines like interleukin-1β, interleukin-6, tumor necrosis factor-alpha, and interleukin-18 have been implicated in its development. These cytokines contribute to PSD through various mechanisms such as HPA axis dysfunction, neurotransmitter alterations, neurotrophic factor changes, gut microbiota imbalances, and genetic predispositions. Understanding the role of cytokines in stroke and PSD may lead to innovative interventions for managing PSD and improving outcomes for stroke survivors experiencing depression.