Will Insig-1 help with a stroke?

A way has been found to reduce damage to brain cells after a strokeElena Novoselova, STRF.ru
Scientists from the Brain Research Center at the University of British Columbia (Canada) have received new data on the mechanism of cell death after a stroke and suggested possible ways to reduce tissue damage.

After a stroke, many brain cells still continue to die, even after blood flow has been restored. Researchers have long known that these mechanisms are triggered by a complex cascade of cellular signals, which as a result lead to the "self-destruction" of brain cells. This time, scientists managed to find out that excessive stimulation of NMDA receptors on the surface of brain cells activates the synthesis of the SREBP-1 protein, which is involved in the cell death program. Usually, the SREBP-1 protein is present in cells throughout the body and participates in cholesterol metabolism.

NMDA receptors control calcium flows through the cell membrane, which are necessary for the normal functioning of brain cells. But after a stroke, the level of glutamate – the most common chemical neurotransmitter – in the cell increases sharply, which leads to hyperstimulation of NMDA receptors that allow excessive concentrations of calcium ions to enter the cell. This leads to rapid degradation of the Insig-1 protein, which can no longer restrain the synthesis of the SREBP-1 protein.

Currently, experts have been able to detect compounds that inhibit SREBP-1 by this particular reaction pathway. The new drug stabilizes Insig-1, and it remains a powerful controller of the concentration of SREBP-1 protein in its active form. A drug tested on animal models was created on the basis of this substance. This made it possible to significantly reduce the number of dying cells.

The results of the research are published in the journal Nature Medicine.

Portal "Eternal youth" http://vechnayamolodost.ru23.11.2009