# Decreased hippocampal neurogenesis and post-stroke depression

## TL;DR

This review explores how reduced brain cell growth in the hippocampus contributes to post-stroke depression and highlights potential treatments.

## Contribution

The paper systematically reviews the role of impaired hippocampal neurogenesis in post-stroke depression and its therapeutic implications.

## Key findings

- Impaired hippocampal neurogenesis is linked to the onset of post-stroke depression.
- Pharmacological and lifestyle interventions show potential in restoring neurogenesis and reducing depressive symptoms.
- Molecular mechanisms like HPA axis dysregulation and neuroinflammation contribute to impaired neurogenesis in PSD.

## Abstract

Post-stroke depression (PSD) is a common and serious complication following stroke, affecting approximately one-third of survivors and contributing to poor functional recovery. Its pathophysiology is multifactorial, with recent evidence highlighting decreased hippocampal neurogenesis as a key mechanistic contributor. This review aims to examine the specific role of hippocampal neurogenesis in PSD, focusing on (1) the evidence linking impaired neurogenesis to PSD onset (2), the underlying molecular and cellular mechanisms—including dysregulation of the hypothalamic–pituitary–adrenal(HPA) axis, neuroinflammation, altered neurotrophic signaling, and neurotransmitter disturbances—and (3) current and emerging therapeutic strategies that promote neurogenesis for PSD management. Pharmacological agents (e.g., antidepressants), neuroregulatory interventions, and lifestyle-based approaches show promise in restoring neurogenic activity and alleviating depressive symptoms. In conclusion, impaired hippocampal neurogenesis represents a central pathway in PSD pathogenesis, offering a valuable target for future research and therapeutic development. Further studies are needed to fully elucidate these mechanisms and translate neurogenesis-focused treatments into clinical practice.