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, July 1, 2019

Muting an inflammatory loudspeaker on immune cells shrinks acute stroke damage

That next step will never occur since your doctors and stroke hospitals will do nothing to contact researchers and push it forward. 

Muting an inflammatory loudspeaker on immune cells shrinks acute stroke damage

Selectively turning down the volume of a "siren" that spurs some angry immune cells to migrate into the brain soon after a stroke could meaningfully reduce symptoms, even days after the stroke
occurs, according to a study (<=details here)in Nature Immunology conducted by neuroscientist Kati Andreasson, MD, and her colleagues.
When the researchers suppressed the activity of a small set of immune cells in mice who'd had strokes, they saw what we'd all like to see more of after such an event: substantially reduced brain damage, better survival rates, and improved motor performance days later. From my news release about the study:
'This new approach worked,' Andreasson said. 'It might mean we can prevent a lot of the brain damage and functional losses that occur after a stroke just by targeting the immune response instead of damaged nerve cells or blood vessels.'
Strokes are the leading cause of disability in the United States because the accompanying brain injury is hard to undo or work around.
"It's a huge problem," Andreasson told me. The best treatments available now, clot-busting drug infusions and clot-removing surgery, are useful only for a fraction of those who experience strokes -- and in many cases only if these interventions are done within the first several hours afterward -- she said.
Again, from my release:
The great majority of strokes occur because a clot lodges in a blood vessel supplying the brain with oxygen and other nutrients. The sudden oxygen cutoff damages the brain tissue dependent on that blood vessel. Once circulation resumes, inflammation-generating breakdown products of dead or dying cells are carried off from the injured brain to distant sites in the body, drawing the attention of immune 'first responders' called myeloid cells that reside mainly in the spleen -- effectively a barracks for immune cells -- and bloodstream. The brain junk jams many of those myeloid cells into inflammatory gear, inducing them to migrate to the brain in search of trouble. .... Inflammation in the brain persists for several days after a stroke, further damaging tissue and compounding patients' loss of function.
But here's the good news: Myeloid cells uniquely feature, on their surfaces, a molecule that acts as an inflammatory loudspeaker. Turning down its volume softens the inflammatory disposition of the immune cells. Andreasson's team learned of an experimental drug that seems to be able to do that -- and it worked, at least in mice.
The next step, of course, is to get it into people who've had strokes and see if it works for us humans, too.

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