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, August 15, 2011

Target for Pain May Also Reduce Brain Injury from Trauma

Another hyperacute option to have your researcher study up on. I may have to have a complete medical bag with all the hyperacute options I've talked about and become my own guinea pig. And hope with a second stroke I am lucid enough to direct my own hyperacute options.
http://www.dddmag.com/Target-for-Pain-May-Also-Reduce-Brain-Injury-from-Trauma-081511.aspx

A peptide that appears to minimize acute and chronic pain was identified as a potential tool to prevent for cell death following traumatic brain injury.

Indiana University School of Medicine researchers show that this peptide short circuits a pathway for chronic pain without interfering with other important nerve functions. Rajesh Khanna, PhD, an assistant professor of pharmacology and toxicology at the IU School of Medicine, and colleagues thought the peptide, CDB3, might be related to cell death in the brain because of another protein it interacts with.

“At least 50 years of research has shown that the NMDA receptor, a protein with well-established links to cell death, gets turned on with injury or trauma leading to massive toxic calcium influx into the cells causing cell death,” Khanna says. “Our strategy was to regulate this protein – to control it but not block it completely since some calcium is needed for fundamental cellular functions.”

The CDB3 peptide spares neurons from death following traumatic brain injury following stroke and accidents. Testing is ongoing as to the usefulness of this peptide in a blast injury model mimics injuries from explosions, motorcycle accidents and other trauma.

Khanna says a single systemic injection of CDB3 allows sufficient peptide to cross the blood-brain barrier and “produces a marked reduction in cell death in the hippocampus, an area important for memory and learning.”

“We’ve extended the function of this peptide beyond pain and the fact that CBD3 protects neurons when given two hours after stroke is very promising,” Khanna adds. The next step in the research is to test the effectiveness of injections of the peptide at longer intervals following injury and with different types of brain injury. The expectation is that targeting the NMDA receptor with this peptide could lead to development of neurotherapeutics against traumatic brain injury as well as other neuronal insults.

The research was published online in the Journal of Biological Chemistry.

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