Study results published recently in the online journal Nature Medicine reveal the discovery of the specific mechanism responsible for the death of brain cells in stroke victims. Researchers had already known that brain cells continue to die even after blood flow had been returned to the brain due to a complex cascade of chemical reactions flows through the brain. What they didn’t know was exactly how and why the brain cells continued to die.
The study¾conducted by researchers at the Brain Research Center of British Columbia¾revealed in animal models that the over-activation of NMDA receptors on the surface of brain cells activates a protein known as SREBP-1, the main culprit responsible for the death of the cells. SREBP-1 is normally found throughout the brain, but is kept in check by another protein, Insig-1.
In the aftermath of a stroke, NMDA receptors become over activated, which leads to a fast breakdown of Insig-1 proteins. The decrease in the mediating presence of Insig-1 forces an increase and activation of SREBP-1, which was shown to be instrumental in the post-stroke death of brain cells. By inhibiting SREBP-1, the scientists involved in the study were able to halt further brain cell death in the animal models.
Dr. Max Cyander, the co-lead of the study, said of the study results, ‘We developed a drug that can stabilize Insig-1, which in turn inhibits the activity of SREBP-1,’ ‘¦ ‘By doing so, we were able to prevent cell death,’ a EurekAlert article reported.
Previous research focused on blocking the NMDA receptors but yielded limited results. The current study demonstrated in animal models that the new drug led to a decrease in the rate and quantity of brain cell death after one month when compared to the levels exhibited in a control group.
The research¾funded by the Heart and Stroke Foundation of BC and Yukon, the Canadian Institutes of Health Research, and the Cure Huntington’s Disease Initiative Foundation¾will be further explored to determine exactly how SREBP-1 leads to cell death, to identify other roles the protein may play in disorders such as Lou Gehrig’s disease, and to develop highly effective treatments for human stroke victims based on the results.