Great Catch-22 here; you need exercise to recover, but you really need 100% recovery to do the required exercises. Have your competent? doctor EXACTLY EXPLAIN HOW TO GET AROUND THAT PROBLEM!
New study sheds light on stroke recovery via exercise-induced migration of mitochondria
Researchers show how exercise protects the brain against stroke by inducing migration of tiny powerhouses through the bloodstream
Peer-Reviewed PublicationCredit: Dr. Toshiki Inaba from Juntendo University School of Medicine, Japahysical 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.(Slight problem here, the penumbra resolves itself into dead brain in the first week, so you need this exercise immediately! HOW THE FUCK WILL YOUR DOCTOR ACCOMPLISH THAT?)
“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.
Reference
Authors | Toshiki Inaba1, Nobukazu Miyamoto1, Kenichiro Hira1, Chikage Kijima1, Yoshifumi Miyauchi1, Hai-Bin Xu1, Kazo Kanazawa1, Yuji Ueno1,2, and Nobutaka Hattori1,3 |
Title of original paper | Mitochondrial intercellular transfer via platelets after physical training exerts neuro-glial protection against cerebral ischemia |
Journal | MedComm |
DOI | |
Affiliations | 1Department of Neurology, Juntendo University School of Medicine, Japan 2Department of Neurology, University of Yamanashi, Japan 3Neurodegenerative Disorders Collaborative Laboratory, RIKEN Center for Brain Science, Japan |
About Assistant Professor Toshiki Inaba
Dr. Toshiki Inaba is a Research Assistant Professor at the Department of Neurology, Juntendo University School of Medicine, Japan. He has over 27 publications to his credit. His areas of research include neurology, systems neuroscience, cerebrovascular physiology, neuroprotection, neuroinflammation, glia, and endothelial dysfunction.
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