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Targeting the muscle-brain axis to improve post-stroke cognition via the FNDC5/irisin/BDNF pathway
Jiating Wei1, Yuangui Cai1, Zimu Jiang1
1Department of Neurology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, PR China; Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, Guangzhou, Guangdong 510080, PR China; National Key Clinical Department and Key Discipline of Neurology, Guangzhou, Guangdong 510080, PR China.
Stroke-induced muscle atrophy disrupts the muscle-brain axis, leading to cognitive impairment. Boosting irisin levels through exercise or gene therapy shows promise for treating post-stroke cognitive dysfunction.
Area of Science:
- Neuroscience
- Muscle Physiology
- Endocrinology
Background:
- The muscle-brain axis, involving FNDC5/irisin/BDNF, is crucial for cognitive function.
- Stroke-induced hemiplegic muscle atrophy may disrupt this axis, contributing to cognitive deficits.
Purpose of the Study:
- To investigate if stroke-related muscle atrophy impairs the FNDC5/irisin/BDNF axis.
- To determine the axis's role in post-stroke cognitive impairment (PSCI).
Main Methods:
- Cross-sectional study of stroke patients and controls, assessing cognition, serum irisin, and muscle MRI.
- Evaluation of muscle atrophy, FNDC5/irisin/BDNF expression, and cognition in stroke models (monkeys, rats).
- Intervention studies using exercise or irisin overexpression to treat PSCI in rats.
Main Results:
- Stroke patients and animal models showed significant muscle atrophy and reduced serum irisin levels.
- Downregulation of FNDC5/irisin/BDNF signaling was observed in atrophic muscles and linked to cognitive decline.
- Exercise or irisin administration improved hippocampal BDNF levels and neurogenesis, alleviating PSCI in rats.
Conclusions:
- Hemiplegic muscle atrophy contributes to PSCI by downregulating the FNDC5/irisin/BDNF axis.
- Elevating irisin presents a potential therapeutic strategy for post-stroke cognitive impairment.
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