Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, January 26, 2026

Nanoscale magnesium hydride alleviates hypoxia-induced myelination deficits in zebrafish

 Can't our fucking failures of stroke associations and stroke medical 'professionals' look at this and see that further research is needed for our myelin damage

Nanoscale magnesium hydride alleviates hypoxia-induced myelination deficits in zebrafish


Li, Jia-Lin1,2,#; Chen, Qiang1,#; Li, Zheng-Hao1,#; Xu, Dao-Jie3; He, Cheng1,*; Liu, Peng1,*

Author Information
Medical Gas Research ():10.4103/mgr.MEDGASRES-D-25-00104, January 23, 2026. | DOI: 10.4103/mgr.MEDGASRES-D-25-00104
  • Open
  • PAP

Abstract

figure1

Defects in myelination impair nerve impulse conduction and functional connectivity, which could lead to cognitive, behavioral and motor deficits in various neurological disorders. Adequate oxygen delivery is vital for brain development, while hypoxia in newborns tends to result in developmental deficiencies in myelination of the brain. The disruption of oligodendrocytes and their progenitor cells caused by hypoxia has been well researched. Nonetheless, the impairing dynamic myelination process is still unclear. Utilizing zebrafish as a model, we established hypoxia via cobalt chloride exposure or low oxygen (8%) incubation. Hypoxia significantly reduced oligodendrocyte progenitor cell numbers in the dorsal spinal cord, impaired migration velocity and suppressed proliferation. Myelination deficits were evident through decreased myelin sheath segment intensity in Tg(MBP:eGFP-CAAX) larvae. Time-lapse imaging revealed compromised dynamic myelination by individual oligodendrocytes under hypoxia, with fewer sheaths and reduced extension rates. Mechanistically, hypoxia elevated reactive oxygen species levels and disrupted mitochondrial membrane potential in cultured rat oligodendrocyte progenitor cells. Nanoscale magnesium hydride, a hydrogen-releasing agent, attenuated these effects. In vivo, magnesium hydride treatment rescued oligodendrocyte progenitor cell numbers and enhanced myelinogenesis capacity in hypoxic zebrafish. These findings demonstrate that magnesium hydride mitigates hypoxia-induced oxidative stress and mitochondrial dysfunction, thereby alleviating myelination deficits.

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