Tau's role in stroke!

Now if we only had a stroke leader to go to to get this researched. The 'leaders' of the WSO - World Stroke Organization, ASA - American Stroke Association, NSA - National Stroke Association have no method to contact them and seem to have no interest in communicating with survivors. This is precisely why I call them fucking failures of stroke associations.  Survivors are fucking screwed until these organizations are destroyed and started up again as survivor led.
This would seem to be able to address the excitotoxity problem in the neuronal cascade of death. If we had ANY person with brains in stroke this would be immediately recognized and a crash research project to make it into a translational intervention. 
http://sciencemission.com/site/index.php?page=news&type=view&id=health-science%2Ftau-s-role-in-stroke&filter=8%2C9%2C10%2C11%2C12%2C13%2C14%2C16%2C17%2C18%2C19%2C20%2C27

Stroke is a major cause of death and disability, and there is only a short window for therapeutic intervention, aimed at restoring blood flow to the brain before neurons are irreversibly damaged.

The study published in Nature Communications finds that mice deficient in tau, a protein within brain cells (neurons), are significantly protected from excitotoxic brain damage after experimental stroke.

"Tau as a drug target is intensively explored in Alzheimer's disease, but as a drug target in stroke is completely new thinking," senior author says.

"That's where our paper has implications beyond mouse model molecular work. Drug development in this space should consider stroke as a disease that you can treat by targeting tau," another author added.

They demonstrate profound protection from brain damage, of more than 90 per cent, in the absence of tau. Authors show that the protection is due to site-specific inhibition of glutamate-induced and Ras/ERK-mediated toxicity by accumulation of Ras-inhibiting SynGAP1, which resides in a post-synaptic complex with tau. Accordingly, reducing SynGAP1 levels in tau−/− mice abolished the protection from pharmacologically induced excitotoxicity and middle cerebral artery occlusion-induced brain damage.

Conversely, over-expression of SynGAP1 prevented excitotoxic ERK activation in wild-type neurons. These findings suggest that tau mediates excitotoxic Ras/ERK signaling by controlling post-synaptic compartmentalization of SynGAP1.

The authors caution that these findings were made in mouse models only, and that pathways to therapies take decades.(Excuses, excuses, once again showing zilch leadership and taking no responsibility in solving anything. Waiting for SOMEONE ELSE TO SOLVE THE PROBLEM?)

https://newsroom.unsw.edu.au/news/health/study-offers-new-mindset-search-stroke-therapies

https://www.nature.com/articles/s41467-017-00618-0