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.

Wednesday, November 28, 2012

Double Duty: Immune System Regulator Found to Protect Brain from Effects of Stroke

My other post on microRNA suggested it was useful for neurogenesis. So demand answers from your doctor or stroke association. Or are you going to let them fail at their job and negatively affect your recovery. Get going, it takes years to get new things thru the medical morass.
http://feeds.sciencedaily.com/~r/sciencedaily/mind_brain/stroke/~3/6wj-03lXm1Y/121128143549.htm
A small molecule known to regulate white blood cells has a surprising second role in protecting brain cells from the deleterious effects of stroke, Johns Hopkins researchers report. The molecule, microRNA-223, affects how cells respond to the temporary loss of blood supply brought on by stroke -- and thus the cells' likelihood of suffering permanent damage.

"We set out to find a small molecule with very specific effects in the brain, one that could be the target of a future stroke treatment," says Valina Dawson, Ph.D., a professor in the Johns Hopkins University School of Medicine's Institute for Cell Engineering. "What we found is this molecule involved in immune response, which also acts in complex ways on the brain. This opens up a suite of interesting questions about what microRNA-223 is doing and how, but it also presents a challenge to any therapeutic application." A report on the discovery is published in the Nov. 13 issue of the Proceedings of the National Academy of Sciences.
RNA is best known as a go-between that shuttles genetic information from DNA and then helps produce proteins based on that information. But, Dawson explains, a decade ago researchers unearthed a completely different class of RNA: small, nimble fragments that regulate protein production. In the case of microRNA, one member of this class, that control comes from the ability to bind to RNA messenger molecules carrying genetic information, and thus prevent them from delivering their messages. "Compared with most ways of shutting genes off, this one is very quick," Dawson notes.
Reasoning that this quick action, along with other properties, could make microRNAs a good target for therapy development, Dawson and her team searched for microRNAs that regulate brain cells' response to oxygen deprivation.
To do that, they looked for proteins that increased in number in cells subjected to stress, and then examined how production of these proteins was regulated. For many of them, microRNA-223 played a role, Dawson says.
In most cases, the proteins regulated by microRNA-223 turned out to be involved in detecting and responding to glutamate, a common chemical signal brain cells use to communicate with each other. A stroke or other injury can lead to a dangerous excess of glutamate in the brain, as can a range of diseases, including autism and Alzheimer's. Because microRNA-223 is involved in regulating so many different proteins, and because it affects glutamate receptors, which themselves are involved in many different processes, the molecule's reach turned out to be much broader than expected, says Maged M. Harraz, Ph.D., a research associate at Hopkins who led the study. "Before this experiment, we didn't appreciate that a single microRNA could regulate so many proteins," he explains.
This finding suggests that microRNA-223 is unlikely to become a therapeutic target in the near future unless researchers figure out how to avoid unwanted side effects, Dawson says.
Other authors on the paper are Stephen M. Eacker, Ph.D., Xueqing Wang, Ph.D., and Ted M. Dawson, M.D., Ph.D., from the Johns Hopkins University School of Medicine.
This work was supported by a grant from the National Institutes of Health (grant DA000266) and by a Maryland Stem Cell Research Fund fellowship.

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