Can 2ME2 improve acute stroke outcomes?
I met a woman who arrived in the hospital yesterday with a devastating stroke to her middle cerebral artery (MCA). It left her unable to speak, with half of her face and body paralyzed. She was among the 3% of stroke victims who arrive in time to receive tPA, less than 3 hours from the onset of symptoms. It worked. She had no bleeding complications. Today she's fine. A miracle of modern medicine snatched her from the jaws of a permanent, devastating neurological injury.
The holy grail of acute stroke therapy has always been to extend the 3 hour window in which clot-busting drugs can be used, so they can reach more than 3% of stroke victims. The problem is that beyond that, too many neurons die, and too many of the remaining ones can not withstand the reperfusion injury, which causes much more harm than the direct ischemic injury. An agent that protects neurons from post-reperfusion inflammatory damage could potentially add hours to the usefulness of tPA and rescue thousands of additional stroke patients every year from the most devastating consequence of their illness.
Chen et al in study published in the Journal of Neurochemistry on 26-May-2007 via early electronic release, demonstrate just such an agent in a rat model of stroke, using 2ME2 combined with tricyclodecan-9-yl-xanthogenate (D609). They conclude, "2ME2 and D609 reduce the infarct volume ... and blood–brain barrier extravasation, decrease the mortality and improve the neurological deficits. In conclusion, 2ME2 and D609 are powerful agents to protect brain from cerebral ischemic injury by inhibiting HIF-1? expression, attenuating the superfluous expression of VEGF to avoid blood–brain barrier disruption and suppressing neuronal apoptosis via BNIP3 pathway."
You can improve your chance of surviving a heart attack by chewing an aspirin. Perhaps the day when you can improve your chance of recovering from a stroke by drinking some Panzem NCD is not far away.
Best Regards,
C-Peptide
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