Exercise and Productive Hippocampal Neurogenesis After Stroke: From Niche Remodeling to Cognitive Recovery

Post-stroke cognitive impairment (PSCI) is a frequent and disabling consequence of stroke that limits long-term recovery and quality of life. Disruption of the hippocampal neurogenic niche may impair adult hippocampal neurogenesis (AHN), while exercise is increasingly recognized as a promising non-pharmacological strategy for cognitive rehabilitation. This review synthesizes evidence that exercise may shift the post-stroke hippocampal niche from a hostile to a permissive state through coordinated regulation of neuroinflammation, neurovascular integrity, and mitochondrial homeostasis. We distinguish increased progenitor proliferation from productive neurogenesis, defined by the survival, maturation, appropriate positioning, and functional integration of newborn neurons. Exercise may attenuate inflammatory signaling, support angiogenesis and blood-brain barrier repair, and improve mitochondrial biogenesis and quality control; however, much of the mechanistic evidence remains preclinical, and increases in early neurogenic markers do not by themselves establish functional neuronal integration or causality. Current clinical evidence supports cognitive benefits of exercise more strongly than it supports AHN as the indispensable mediator of those benefits. A productive-neurogenesis framework therefore provides a more rigorous basis for interpreting existing studies and designing future experiments that combine lineage tracing, temporally controlled neurogenesis ablation, circuit-level analysis, and domain-specific cognitive outcomes.