Showing posts with label oligodendrocytes. Show all posts
Showing posts with label oligodendrocytes. Show all posts
Friday, May 8, 2026
Tuesday, January 27, 2026
Mitochondria magic: Exercise’s value soars with this news
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!
I can almost guarantee your doctor and hospital will KNOW NOTHING AND DO NOTHING!
No human research will occur; nothing will be done! That is how fucking incompetent the whole stroke medical world is. Hopefully comeuppance will hit them all with a stroke. And they can regret their incompetence in not solving stroke to 100% recovery!
Al this incompetence is a result of NO leadership firing the incompetent persons!
Mitochondria magic: Exercise’s value soars with this news
Japanese researchers found that exercise triggers muscle cells to send mitochondria through the bloodstream to protect and repair brain tissue after stroke
Scientists at Juntendo University School of Medicine have uncovered a remarkable process that explains how exercise protects the brain from stroke damage. The research team discovered that physical activity triggers muscle cells to produce mitochondria that travel through the bloodstream and deliver healing benefits directly to injured brain tissue.
The study, published in the journal MedComm on Jan. 15, reveals that blood platelets act as tiny transport vehicles, carrying these cellular powerhouses from muscles to the brain. Once they arrive, the mitochondria help damaged neurons survive oxygen deprivation and support the repair of critical brain structures. The findings could eventually lead to new treatments for stroke patients who are too frail to exercise on their own.(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?)
Research Assistant Professor Toshiki Inaba led the investigation alongside colleagues Nobukazu Miyamoto and Nobutaka Hattori at Juntendo’s Department of Neurology. The team conducted experiments using mouse models designed to replicate both stroke and dementia conditions, providing insights into how cellular communication might be harnessed for therapeutic purposes.
Watching mitochondria travel between cells
Miyamoto’s interest in mitochondrial migration began during a research fellowship at Massachusetts General Hospital and Harvard Medical School, where he first observed these cellular structures moving from one cell to another. That observation sparked the realization that mitochondrial transfer might offer treatment possibilities for various neurological conditions.
For the current study, researchers divided mice into groups and had some perform low-intensity treadmill exercise while others remained sedentary. The team then carefully tracked brain damage, movement abilities, memory function and changes in brain and muscle cells among both groups. They also measured mitochondrial levels and activity throughout the experiment.
The results showed clear advantages for the mice that exercised. These animals experienced less damage to white matter and myelin, the protective coating around nerve fibers. They also demonstrated better memory retention and movement capabilities compared to sedentary mice, while experiencing fewer complications following stroke events.
Platelets serve as cellular delivery system
The research revealed that exercise significantly increased mitochondrial production in both muscle tissue and the bloodstream. Blood platelets, typically known for their role in clotting, took on an unexpected function by capturing mitochondria from muscle cells and transporting them to the brain.
Once in the brain, these traveling mitochondria didn’t just reach neurons. They also made their way to support cells including oligodendrocytes, which produce protective myelin, and astrocytes, star-shaped cells that help form the blood-brain barrier. The mitochondria provided crucial support to cells in the damaged area and the surrounding region called the penumbra, where brain tissue remains vulnerable but potentially salvageable.
Inside these brain cells, the delivered mitochondria helped them endure low-oxygen conditions that typically cause widespread cell death after stroke. They supported the repair of white matter, the brain’s communication infrastructure, and reduced the cascade of complications that often follow stroke events.
Limited options drive search for new approaches
Current stroke treatment relies heavily on clot removal or dissolution, but these interventions only work within a narrow window after symptoms begin. Once that critical time frame passes, patients face limited therapeutic options. Physical rehabilitation and symptom management become the primary focus, yet many stroke survivors continue struggling with walking difficulties, speech problems and memory decline.
Exercise has long been recognized as beneficial for both stroke prevention and recovery. However, many stroke patients are elderly and lack the physical stamina required to exercise intensively enough to gain those protective benefits. This reality makes the search for alternative approaches particularly urgent.
Inaba acknowledged that while the research team has identified several technical and biological challenges through additional experiments, the approach holds promise for reducing neurological problems after stroke. The applications might extend beyond stroke to include mitochondrial diseases and related neurodegenerative conditions where current treatment options remain limited.
From mice to potential human therapies
The pathway from laboratory findings to clinical treatments typically spans years and requires extensive testing for safety and effectiveness. If the mitochondrial transfer approach proves successful in human trials, it could potentially allow stroke patients to receive the benefits of exercise through transfusions of platelet preparations enriched with mitochondria.
Such a treatment would be particularly valuable for patients who cannot engage in physical rehabilitation due to age, frailty or the severity of their condition. The approach might also offer hope for preventing the progression of vascular dementia, a condition that currently has no established treatments.
The research team’s work builds on growing scientific understanding of how cells communicate and share resources. By revealing the specific mechanism through which exercise protects the brain, the scientists have opened a new avenue for developing therapies that could help millions of stroke survivors worldwide maintain better neurological function and quality of life.
SOURCE: juntendo
Friday, January 23, 2026
New study sheds light on stroke recovery via exercise-induced migration of mitochondria
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!
I can almost guarantee your doctor and hospital will KNOW NOTHING AND DO NOTHING!
No human research will occur; nothing will be done! That is how fucking incompetent the whole stroke medical world is. Hopefully comeuppance will hit them all with a stroke. And they can regret their incompetence in not solving stroke to 100% recovery!
Al this incompetence is a result of NO leadership firing the incompetent persons!
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 Publication“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.
Friday, October 31, 2025
Oligodendrocyte progenitor cells promote blood vessel growth after stroke
All this earlier information on blood vessel growth! Did your incompetent? doctor get protocols created in the past 15 years?- oligodendrocytes (30 posts to May 2012)
-
blood vessel formation
(5 posts to April 2016)
-
angiogenesis
(140 posts to April 2011)
Oligodendrocyte progenitor cells promote blood vessel growth after stroke
Stroke is a leading cause of death and disability, affecting 1 in 4 people during their lifetime. Stroke happens when blood vessels in the brain get clogged or damaged, impairing blood flow and oxygen supply to the brain, which leads to death of neurons and other brain cells. Although brain damage can be limited by interventions to restore blood flow, most stroke survivors experience some lifelong impairments of e.g. speech, movement, or cognitive function.
Despite the existence of immature stem cells in the brain, their role in repair is uncertain and the brain's ability to recover from stroke remains limited. Takakuni Maki, Ken Yasuda, Kazuto Tsukita, and colleagues from Kyoto University, Japan, have now demonstrated that oligodendrocyte progenitor cells (OPCs)-a well-known immature glial cell type in the brain-can promote new blood vessel formation after stroke under hypoxic conditions. The research was published today in Stem Cell Reports.
The researchers found that OPCs, whose normal task is to differentiate into oligodendrocytes that form an insulating layer around axons to support neuronal function, among other roles, can change their behavior under conditions of extremely low oxygen, such as in stroke areas in the brain, and start to interact with blood vessels to stimulate their growth. The researchers were able to demonstrate this connection when they exposed mouse OPCs in the lab to very low oxygen levels simulating stroke. When injected into the blood circulation of mice with stroke, the OPCs migrated to the stroke region and survived there for several weeks. Critically, the low oxygen-conditioned OPCs more effectively helped to limit the damage to brain tissue and partially restored movement and behavior compared with unconditioned OPCs. This was likely due to the extensive formation of new blood vessels, which is critical for restoring oxygen and nutrient supply to brain cells, found in stroke brains treated with low oxygen-conditioned OPCs.
More research will be required to confirm these results and test if low oxygen-conditioned OPCs are safe and effective to be used in patients, potentially in combination with standard interventions to promote blood flow and re-oxygenation.
Source:Journal reference:Kuwata, Y., et al. (2025). Characterizing hypoxia-orchestrated post-stroke changes in oligodendrocyte precursor cells for optimized cell therapy. Stem Cell Reports. doi.org/10.1016/j.stemcr.2025.102687
- oligodendrocytes (30 posts to May 2012)
- blood vessel formation (5 posts to April 2016)
- angiogenesis (140 posts to April 2011)
Stroke is a leading cause of death and disability, affecting 1 in 4 people during their lifetime. Stroke happens when blood vessels in the brain get clogged or damaged, impairing blood flow and oxygen supply to the brain, which leads to death of neurons and other brain cells. Although brain damage can be limited by interventions to restore blood flow, most stroke survivors experience some lifelong impairments of e.g. speech, movement, or cognitive function.
Despite the existence of immature stem cells in the brain, their role in repair is uncertain and the brain's ability to recover from stroke remains limited. Takakuni Maki, Ken Yasuda, Kazuto Tsukita, and colleagues from Kyoto University, Japan, have now demonstrated that oligodendrocyte progenitor cells (OPCs)-a well-known immature glial cell type in the brain-can promote new blood vessel formation after stroke under hypoxic conditions. The research was published today in Stem Cell Reports.
The researchers found that OPCs, whose normal task is to differentiate into oligodendrocytes that form an insulating layer around axons to support neuronal function, among other roles, can change their behavior under conditions of extremely low oxygen, such as in stroke areas in the brain, and start to interact with blood vessels to stimulate their growth. The researchers were able to demonstrate this connection when they exposed mouse OPCs in the lab to very low oxygen levels simulating stroke. When injected into the blood circulation of mice with stroke, the OPCs migrated to the stroke region and survived there for several weeks. Critically, the low oxygen-conditioned OPCs more effectively helped to limit the damage to brain tissue and partially restored movement and behavior compared with unconditioned OPCs. This was likely due to the extensive formation of new blood vessels, which is critical for restoring oxygen and nutrient supply to brain cells, found in stroke brains treated with low oxygen-conditioned OPCs.
More research will be required to confirm these results and test if low oxygen-conditioned OPCs are safe and effective to be used in patients, potentially in combination with standard interventions to promote blood flow and re-oxygenation.
Source:
Journal reference:
Kuwata, Y., et al. (2025). Characterizing hypoxia-orchestrated post-stroke changes in oligodendrocyte precursor cells for optimized cell therapy. Stem Cell Reports. doi.org/10.1016/j.stemcr.2025.102687
Saturday, September 6, 2025
Fujian tablet regulates the Foxo3a/GPX4 axis to promote remyelination and improve motor function in ischemic stroke
Your competent? doctor KNOWS EXACTLY HOW MUCH DEMYELINATION HAS OCCURRED and has EXACT PROTOCOLS TO FIX THAT! RIGHT? NO? So your doctor knows nothing and is completely fucking incompetent? Will your doctor once again prove incompetence by not getting human testing done?
demyelination
(10 posts to November 2013)
demyelinating
(24 posts to May 2012)
myelination
(8 posts to May 2016)
myelin-associated inhibitors
(1 post to February 2017)
myelin-associated glycoprotein
(1 post to May 2015)
Fujian tablet regulates the Foxo3a/GPX4 axis to promote remyelination and improve motor function in ischemic stroke
Subscribe to:
Posts (Atom)