Physical rehabilitation and symptom management remain crucial in treating stroke patients, as clot removal or dissolution is only effective within a narrow time frame after the event. Beyond this period, many patients face long-term challenges such as difficulty in walking, speaking, and memory decline. While exercise is known to prevent strokes and aid recovery, many elderly patients are too frail to exercise sufficiently to reap these benefits.
In an innovative study published in the journal MedComm on January 15, 2026, 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, explored how exercise biologically protects the brain against stroke through mitochondrial migration.
Mitochondrial Migration: A New Frontier in Stroke Recovery
Dr. Miyamoto explains, “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.”
The research team utilized mouse models mimicking stroke and dementia. Some mice from both groups were subjected to low-intensity treadmill exercise. The researchers then assessed brain damage, movement, memory, and changes in brain and muscle cells, alongside mitochondrial dosage and activity, comparing mice that exercised with those that did not.
Exercise and Brain Health: The Biological Mechanism
Mice that underwent treadmill exercise exhibited significant benefits, including reduced damage to white matter and myelin, improved 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 functioned like delivery vehicles, transporting mitochondria produced in muscle cells to brain cells, including neurons and support cells such as oligodendrocytes and astrocytes. Once in the brain, these mitochondria aided brain cells in the damaged area and the surrounding penumbra, helping them survive under low-oxygen conditions, supporting white matter repair, and reducing post-stroke complications.
Implications for Future Treatments
Dr. Inaba highlights the potential impact of this research: “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.”
This pioneering study opens up exciting possibilities for new treatments for stroke recovery and the prevention of vascular dementia, and potentially other debilitating diseases that cause brain cell degeneration. If found safe and successful in human trials, the benefits of exercise could be harnessed through the transfusion of mitochondria-laden platelets.
Looking Ahead: The Path to Human Trials
The announcement comes as a beacon of hope for those affected by stroke and related conditions. The next steps involve rigorous testing to ensure the safety and efficacy of this approach in human subjects. Should these trials prove successful, the medical community could witness a paradigm shift in how stroke recovery and neurodegenerative diseases are treated.
Dr. Toshiki Inaba, a Research Assistant Professor at the Department of Neurology, Juntendo University School of Medicine, Japan, has over 27 publications to his credit. His research spans neurology, systems neuroscience, cerebrovascular physiology, neuroprotection, neuroinflammation, glia, and endothelial dysfunction, positioning him as a leading figure in this groundbreaking study.
