לוח שנה משולב

Numerous clinical and preclinical investigators have reported that in several important medical indications such as in (i) ischemic stroke, (ii) traumatic brain injuries (TBI), (iii) acute migraine cases, (iv) glioblastoma brain tumors and (v) epileptic attacks, there is a rapid accumulation in the brain of excess glutamate molecules which are excitotoxic and this leads to significant neurological damage and motoric incapacitations in patients.
Vivian Teichberg introduced a method for scavenging of excess brain glutamate which consists of the intravenous administration of a recombinant preparation of the enzyme, Glutamate Oxaloacetate Transaminase (GOT). This causes a rapid decrease in blood glutamate levels and creates a gradient which leads to the efflux of the excess brain glutamate into the blood stream and reduces neurological damage.
The main advantage of the Brain Glutamate Scavenging technology, over other drug treatments that are currently being developed, is that the augmentation of GOT activity occurs in the blood circulation and therefore, doesn’t affect normal brain neurophysiology, whereas the pharmacological inhibition of the activities of glutamate receptors or transport systems occurs in the brain, and could be followed by serious side effects in the central nervous system.

Stroke is a leading cause of death and long-term disability. In this talk, I will describe how a mild sensory stimulation (e.g., single whisker, tone) delivered to a rodent model of ischemic stroke (permanent occlusion of a major artery supplying blood to the cortex) can completely protect the cortex from an impending stroke. The mechanism underlying this surprising protection was revealed to be a new type of activity-dependent neurovascular plasticity. These findings will be presented in the context of our new understanding regarding the very large spread of evoked activity in sensory cortex supported by an underlying network of extremely long-range horizontal projections.