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 2, 2011

Cypin protein could prevent secondary damage after stroke

More hyperacute options for your researcher.
http://www.sciencecodex.com/read/rutgers_neuroscientist_says_protein_could_prevent_secondary_damage_after_stroke-80802

One of two proteins that regulate nerve cells and assist in overall brain function may be the key to preventing long-term damage as a result of a stroke, the leading cause of disability and third leading cause of death in the United States.

In a recent study published in the Journal of Neuroscience, Bonnie Firestein, professor of cell biology and neuroscience, in the School of Arts and Sciences, says the new research indicates that increased production of two proteins – cypin and PSD-95 – results in very different outcomes.

While cypin – a protein that regulates nerve cell and neuron branching critical to normal brain functioning -- prevents nerve cells not damaged during the initial stroke from losing the ability to communicate with other cells and halts any secondary brain or neurological damage, PSD-95 accelerates cell destruction and inhibits recovery. Secondary injury from a stroke can occur days or even weeks after the injury and often includes a lack of blood flow, insufficient oxygen, and swelling of the brain.

"We don't know how or why cypin acts during this process, but what we do know is that cypin helps nerve cells survive," said Firestein, who first isolated and identified cypin more than a decade ago. Since then, she has been researching how it works in the brain and could be used to treat traumatic brain injury and other serious neurological disorders.

Firestein and her former graduate student Chia-Yi Tseng conducted the laboratory research by putting nerve cells in a dish and creating an "experimental stroke" – mimicking a massive amount of glutamate released, resulting in nerve cells destroyed.

They wanted to determine if anything could be done to stop the secondary damage that occurs after a stroke and discovered that while a greater number of neurons that survived the stroke were spared secondary destruction with increased amounts of cypin, too much PSD-95 resulted in the death of nerve cells not damaged inititally.

"I would hope that this research aids in the development of an effective therapeutic intervention, saving neurons and reducing the long-term effects of stroke and other traumatic brain injuries," said Firestein.

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