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Muscle-Derived Small Extracellular Vesicles Mediate Exercise-Induced Cognitive Protection in Chronic Cerebral

Huawei Lin^1,2, Lianhua Yin³, Weilin Liu^2,4,5

¹College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, 350122, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|April 24, 2025

Summary

Exercise releases muscle-derived extracellular vesicles carrying miR-17/20a-5p, which communicate with the brain to improve cognitive function and synaptic plasticity, particularly in chronic cerebral hypoperfusion.

Keywords:

exercise extracellular vesicles miRNAs synaptic plasticity vascular cognitive impairment

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Published on: May 4, 2015

Area of Science:

Neuroscience
Exercise Physiology
Molecular Biology

Background:

Physical exercise is neuroprotective against cognitive impairment from chronic cerebral hypoperfusion (CCH).
Mechanisms of exercise-induced muscle-to-brain signaling are not fully understood.

Purpose of the Study:

To elucidate the role of muscle-derived extracellular vesicles (sEVs) in mediating exercise's cognitive benefits.
To identify specific molecular signals involved in exercise-induced muscle-brain communication.

Main Methods:

Systematic delivery of muscle-derived sEVs to CCH models.
miRNA sequencing of sEVs.
Molecular analysis of the mTOR pathway in the hippocampus.
Genetic manipulation of DEPTOR and mTOR in vivo.

Main Results:

Muscle-derived sEVs enhance synaptic plasticity and cognitive function in CCH.
miR-17/20a-5p within sEVs are key mediators of this crosstalk.
miR-17/20a-5p activate the hippocampal mTOR pathway via DEPTOR.
Depletion of miR-17/20a-5p or DEPTOR overexpression impairs exercise benefits.

Conclusions:

Muscle-derived sEVs carrying miR-17/20a-5p act as exercise-induced myokines.
The miR-17/20a-5p/DEPTOR/mTOR pathway is critical for exercise-mediated cognitive enhancement.
Targeting this pathway offers therapeutic potential for cognitive impairment.