Mitochondrial Intercellular Transfer via Platelets After Physical Training Exerts Neuro-Glial Protection Against...

Area of Science:

• Neuroscience
• Cell Biology
• Exercise Physiology

Background:

• Thrombolytic therapy for stroke is limited by time constraints.
• Sarcopenia, common in aging populations, can impede stroke recovery.
• Mitochondria's role in cellular health and potential therapeutic applications are under investigation.

Purpose of the Study:

• To investigate the role of exercise-induced mitochondrial migration from muscle to the brain in stroke recovery.
• To explore the therapeutic potential of muscle-derived mitochondria in mitigating stroke-related brain injury and cognitive deficits.

Main Methods:

• Utilized mouse models of chronic hypoperfusion and acute ischemia.
• Conducted in vitro studies using rat primary cells under oxygen-glucose deprivation.
• Assessed the effects of treadmill exercise and mitochondrial transfer on white matter integrity, glial activation, and neurological function.

Main Results:

• Treadmill exercise protected against white matter injury, myelin loss, and memory deficits in hypoperfusion models.
• Exercise training reduced glial activation and post-stroke complications in acute ischemia models.
• Muscle-derived mitochondria, transported via platelets, enhanced neuronal, astrocyte, and oligodendrocyte survival and improved outcomes in ischemic white matter injury.

Conclusions:

• Exercise promotes mitochondrial migration from muscle, which confers neuroprotection and aids stroke recovery.
• Muscle-derived mitochondria, acting as a critical part of the secretome, may mediate the benefits of remote ischemic preconditioning.
• Cell-to-cell mitochondrial migration presents a promising strategy for reducing post-stroke complications and vascular dementia.