While thrombolytic therapy remains one of the most effective strategies for stroke recovery, it is effective only for a short span of time. Now, researchers from Japan have demonstrated how numerous mitochondria, the powerhouses of the cell, produced by muscles during physical training, can aid in stroke recovery.
The cell-to-cell transfer of these mitochondria, via the blood platelets, protected mouse brain cells in conditions, such as stroke and certain dementias, offering a novel therapeutic approach.
Physical rehabilitation and symptom management still remain the mainstay of treatment for stroke, as clot removal or dissolution is effective only within a narrow time frame after the stroke. After that, many patients are left with long-term problems like difficulty in walking, speaking, and memory decline. Exercise has been beneficial in preventing strokes and improving recovery. However, the majority of these patients, being elderly, are too frail to exercise enough to gain these benefits.
In an innovative study published in the journal MedComm on January 15, 2026, a team of researchers led by Research Assistant Professor Toshiki Inaba from the Department of Neurology, Juntendo University School of Medicine, Japan, along with Dr. Nobukazu Miyamoto and Dr. Nobutaka Hattori from Juntendo University School of Medicine, Japan, explored how exercise protects the brain against stroke at a biological level through mitochondrial migration.
“It was during my research fellowship with Assistant Professor Kazuhide Hayakawa at Massachusetts General Hospital/Harvard Medical School that I first observed that these mitochondria could travel from one cell to another, leading to the realization that mitochondrial transfer could be harnessed for a wide range of therapeutic applications. This motivated us to explore intercellular mitochondrial transfer as a novel treatment strategy,” explains Dr. Miyamoto.
The team used mouse models that mimic stroke as well as dementia. Some mice from both these groups were then made to perform low-intensity treadmill exercise. The researchers then compared brain damage, movement, memory, and changes in brain, muscle cells, and mitochondrial dosage and activity among the mice that exercised and those that did not. Mice that underwent treadmill exercise showed clear benefits, such as less damage to the white matter and myelin, better memory and movement, and mitigation of post-stroke complications.
Notably, exercise increased mitochondrial levels in muscle and blood, facilitating their migration between tissues via platelets. The platelets acted like delivery trucks, carrying mitochondria produced in the muscle cells to the brain cells, including neurons and their support cells, such as the protective myelin-forming cells (oligodendrocytes) and the star-shaped astrocytes, which form a protective barrier between the blood and the brain. Once in the brain, these mitochondria helped brain cells in the damaged area, as well as in the surrounding region, called the penumbra, survive under low-oxygen conditions, supported repair of white matter, and reduced post-stroke complications.
“Currently, there are limited effective therapies for reducing post-stroke neurological sequelae, and no established treatments to prevent the progression of vascular dementia. Although additional experiments have revealed several technical and biological challenges, the proposed approach has the potential to contribute to a future in which neurological sequelae after cerebral infarction can be mitigated. Moreover, the therapeutic applications may extend beyond stroke to mitochondrial diseases and related neurodegenerative disorders,” says Dr. Inaba.
This pioneering study opens up exciting possibilities for new treatments for stroke recovery and prevention of vascular dementia, and possibly other debilitating diseases that cause brain cell degeneration. If found safe and successful in human trials, the benefits of exercise could be reaped through the transfusion of mitochondria-laden platelets.
