Exercise-Induced Irisin Signaling in Hippocampal Ischemic Stroke: Mechanisms of Neuroplasticity and Cognitive Recovery
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Abstract
Ischemic stroke decreases cerebral blood flow, injuring CNS. Necrotic core and ischemic penumbra forms, with further injury via excitotoxicity, oxidative stress, neuroinflammation, and BBB disruption. Hippocampal injury leads to post-stroke cognitive dysfunction. Exercise improves cardiovascular, functional, and cognitive outcomes post-stroke, and aerobic exercise is the primary driver of cognitive improvement compared to resistance and multimodal. Repeated moderate-intensity aerobic exercise initiated early post-stroke yields the most consistent cognitive outcomes. Irisin, derived from FNDC5 and released during exercise, is a critical neuroprotective myokine. Irisin reduces COX-2, NFκB, TNF-α, and IL-6, thereby decreasing neuroinflammation and neuronal injury,¹while increasing BDNF, promoting neurogenesis, synaptic regeneration, and neuronal survival. Exercise increases irisin which increases BDNF, improving neuroplasticity and cognitive recovery.
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Affiliations
- California Health Sciences University College of Osteopathic Medicine