Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 27,818 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective 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.
Friday, September 28, 2018
Astrocyte-Derived Exosomes Treated With a Semaphorin 3A Inhibitor Enhance Stroke Recovery via Prostaglandin D2 Synthase
Have your doctor and stroke hospital follow this up with the researchers they work with for human testing. Or are they going to be incompetent like usual and DO NOTHING?
Exosomes
play a pivotal role in neurogenesis. In the peri-infarct area after
stroke, axons begin to regenerate but are inhibited by astrocyte scar
formation. The direct effect and underlying molecular mechanisms of
astrocyte-derived exosomes on axonal outgrowth after ischemia are not
known.
Methods—
Using
a semaphorin 3A (Sema3A) inhibitor, we explored neuronal signaling
during axonal outgrowth after ischemia in rats subjected to middle
cerebral artery occlusion and in cultured cortical neurons challenged
with oxygen-glucose deprivation. Furthermore, we assessed whether this
inhibitor suppressed astrocyte activation and regulated
astrocyte-derived exosomes to enhance axonal outgrowth after ischemia.
Results—
In
rats subjected to middle cerebral artery occlusion, we administered a
Sema3A inhibitor into the peri-infarct area from 7 to 21 days after
occlusion. We found that phosphorylated high-molecular weight
neurofilament-immunoreactive axons were increased, glial fibrillary
acidic protein–immunoreactive astrocytes were decreased, and functional
recovery was promoted at 28 days after middle cerebral artery occlusion.
In cultured neurons, the Sema3A inhibitor decreased Rho family GTPase
1, increased R-Ras, which phosphorylates Akt and glycogen synthase
kinase 3β (GSK-3β), selectively increased phosphorylated GSK-3β in
axons, and thereby enhanced phosphorylated high-molecular weight
neurofilament-immunoreactive axons after oxygen-glucose deprivation. In
cultured astrocytes, the Sema3A inhibitor suppressed activation of
astrocytes induced by oxygen-glucose deprivation. Exosomes secreted from
ischemic astrocytes treated with the Sema3A inhibitor further promoted
axonal elongation and increased prostaglandin D2 synthase expression on microarray analysis. GSK-3β+ and prostaglandin D2 synthase+ neurons were robustly increased after treatment with the Sema3A inhibitor in the peri-infarct area.
Conclusions—
Neuronal
Rho family GTPase 1/R-Ras/Akt/GSK-3β signaling, axonal GSK-3β
expression, and astrocyte-derived exosomes with prostaglandin D2 synthase expression contribute to axonal outgrowth and functional recovery after stroke.
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