New information about the mechanism that leads to the destruction of brain cells following a stroke, as well as a possible way to mitigate that damage has been revealed by researchers at the Brain Research Centre.
After a stroke, many brain cells continue to die even after blood flow has been restored.
Researchers have long known that this is due to a complicated cascade of cellular messages that lead to the "self-destruction" and death of brain cells.
In the new study, it was discovered that, in animal models, the over-activation of NMDA receptors-special receptors on the surface of brain cells-activates another protein, called SREBP-1, which subsequently causes cell death.
SREBP-1 is found naturally in cells throughout the body and is involved with cholesterol and other fat production.
NMDA receptors control the movement of calcium in and out of brain cells, which is necessary for normal brain function.
But, after a stroke, levels of glutamate-the most abundant chemical messenger in the brain-rise rapidly in cells, leading to over-activation of NMDA receptors, an excess of calcium entering cells, and the onset of cell death.
The researchers found that under normal conditions, SREBP-1 is largely kept in an inactive form by a protein known as Insig-1.