A method developed by Weizmann researchers could accelerate recovery from stroke and head trauma, two new studies out of Spain have said.
Much of the devastation of stroke and head trauma is due to damage caused by the overproduction of a substance in the brain called glutamate.
Until now, preventing this damage has been impossible as many drugs don't cross the so-called blood-brain barrier, and those that do often don't work as intended.
But a method originally devised at the Weizmann Institute of Science may, in the future, offer a way to avert such glutamate-induced harm.
Prof Vivian I. Teichberg of the institute's Neurobiology Department first demonstrated a possible way around these problems in 2003.
Glutamate - a short-lived neurotransmitter - is normally all but absent in brain fluids.
After a stroke or injury, however, the glutamate levels in brain fluid become a flood that over-excites the cells in its path and kills them.
Instead of attempting to get drugs into the brain, Teichberg had the idea that one might be able to transport glutamate from the brain to the blood using the tiny 'pumps', or transporters, on the capillaries that work on differences in glutamate concentration between the two sides.
He thought that a naturally-occurring enzyme called glutamate-oxaloacetate transaminase (GOT, for short) could 'scavenge' blood glutamate, significantly lowering its levels.
Two new studies, conducted by Fransisco Campos and others from the lab of Prof Jose Castillo in the University of Santiago de Compostela, Spain, now provide a definitive demonstration of Teichberg's results.
In the first, the scientists conclusively showed that oxoloacetate injected into rats with stroke-like brain injuries reduces glutamate levels both in the blood and in the affected brain region, while significantly lessening both cell death and the swelling that can accompany stroke.
In the second, a team of neurologists in two different hospitals checked the levels of glutamate and GOT in several hundred stroke victims who were admitted to their hospitals.
They found that the most significant predictor of the prognosis - how well they would recover at three months and how much brain damage they would suffer - was the levels of these two substances. High glutamate levels correlated with a poor outcome, high GOT levels with a better one.
The overall implication of these two papers is that administering GOT might improve a patient's chances of recovering, as well as speeding up the process.