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 22, 2014

Regulatory T Cells in Central Nervous System Injury: A Double-Edged Sword

I don't understand, but what is your doctor doing with this information?
http://www.ncbi.nlm.nih.gov/pubmed/25320276

Abstract

Previous research investigating the roles of T effector (Teff) and T regulatory (Treg) cells after injury to the CNS has yielded contradictory conclusions, with both protective and destructive functions being ascribed to each of these T cell subpopulations. In this work, we study this dichotomy by examining how regulation of the immune system affects the response to CNS trauma. We show that, in response to CNS injury, Teff and Treg subsets in the CNS-draining deep cervical lymph nodes are activated, and surgical resection of these lymph nodes results in impaired neuronal survival. Depletion of Treg, not surprisingly, induces a robust Teff response in the draining lymph nodes and is associated with impaired neuronal survival. Interestingly, however, injection of exogenous Treg cells, which limits the spontaneous beneficial immune response after CNS injury, also impairs neuronal survival. We found that no Treg accumulate at the site of CNS injury, and that changes in Treg numbers do not alter the amount of infiltration by other immune cells into the site of injury. The phenotype of macrophages at the site, however, is affected: both addition and removal of Treg negatively impact the numbers of macrophages with alternatively activated (tissue-building) phenotype. Our data demonstrate that neuronal survival after CNS injury is impaired when Treg cells are either removed or added. With this exacerbation of neurodegeneration seen with both addition and depletion of Treg, we recommend exercising extreme caution when considering the therapeutic targeting of Treg cells after CNS injury, and possibly in chronic neurodegenerative conditions.

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