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, October 5, 2011

Study eyes EP4 receptors for stroke treatment

Sounds like another therapy that can stop parts of the cascade of neuronal death, lets getcracking on trials.
http://www.stanforddaily.com/2011/10/05/study-eyes-ep4-receptors-for-stroke-treatment/

A School of Medicine study, led by neurology professor Katrin Andreasson, suggests that a new treatment for strokes could be realized by focusing on a receptor in nerve and endothelial cells which, when simulated, releases a chemical that helps to dilate blood vessels and improve blood flow. The study, performed on mice, was published last Monday in the online Journal of Clinical Investigation.

The study started by investigating a class of drugs called COX-2-selective inhibitors. Once a spark of promise within the medical community, COX-2 selective inhibitors were believed to have the effects of aspirin without the stomach pain. However, the inhibitors ended up contributing to what it was supposed to prevent: in clinical trials, those taking the drug actually experienced an increased risk of heart attacks and strokes.

The drug functions as a pain reliever by helping to hinder the production of a type of messenger molecule called prostaglandin. Prostaglandins travel from cell to cell, triggering different activities within the cells they land on and bind to. One specific type of prostaglandin, called PGE2, is linked to causing pain and inflammation. In a School of Medicine press release, Andreasson said that her team wanted to see why COX-2-selective inhibitors caused strokes instead of curbing them.

They discovered that PGE2 has four different receptors, and one of these, EP4, causes an increase of nitric oxide, a chemical that helps to relax blood muscles and enhance blood flow, when activated. Mice which were injected with EP4 three hours after a stroke experienced less brain damage.

“We showed that activating this single receptor, EP4, three hours after a stroke not only diminishes the volume of a mouse’s affected brain tissue but also enhances the mouse’s functional recovery,” Andreasson said in the statement. “And we’ve taken this a step further by diligently unraveling the mechanisms by which that happens.”

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