Washington, Jan 22 (ANI): A group of scientists has identified a way to block a "cell death signal" that they believe triggers brain damage during strokes.
The finding was made by biomedical scientists from the University of Central Florida and Louisiana State University.
Strokes, also known as cerebral ischemia, are caused by inadequate blood flow to the brain.
In the study, boffins focused on a neurotransmitter that typically plays an important role in communication among nerve cells in the brain and fosters learning and memory. This glutamate neurotransmitter opens the NMDA (N-methyl-D-aspartate) receptors, allowing the entry of calcium into the nerve cells.
Under normal conditions, the activity of the NMDA receptors is tightly regulated to prevent nerve cells from becoming overloaded with calcium. During a stroke, however, that process of regulation breaks down. The excessive influx of calcium through NMDA receptors kills the nerve cells and can cause severe brain damage.
Striving to prevent such calcium overloads, the research team discovered that an enzyme, DAPK1 (Death-Associated Protein Kinase 1), binds to a portion of the NMDA receptor and acts as a "cell death signal" during strokes.
Researchers hypothesized that by preventing DAPK1 from binding with the NMDA receptors, they could prevent the calcium overloads and cell deaths. They developed a potent compound to test their theory and found that the compound blocked DAPK1, protecting brain cells against stroke injury, and did not affect the beneficial physiological functions of the receptors.
"It is conceivable that this study not only provides new insights into the cellular and molecular basis responsible for stroke damage, but also provides a therapeutic target for stroke therapy," said Youming Lu, the LSU professor who led the team of scientists.
The findings appear in the Jan. 22 issue of Cell. (ANI)
The finding was made by biomedical scientists from the University of Central Florida and Louisiana State University.
Strokes, also known as cerebral ischemia, are caused by inadequate blood flow to the brain.
In the study, boffins focused on a neurotransmitter that typically plays an important role in communication among nerve cells in the brain and fosters learning and memory. This glutamate neurotransmitter opens the NMDA (N-methyl-D-aspartate) receptors, allowing the entry of calcium into the nerve cells.
Under normal conditions, the activity of the NMDA receptors is tightly regulated to prevent nerve cells from becoming overloaded with calcium. During a stroke, however, that process of regulation breaks down. The excessive influx of calcium through NMDA receptors kills the nerve cells and can cause severe brain damage.
Striving to prevent such calcium overloads, the research team discovered that an enzyme, DAPK1 (Death-Associated Protein Kinase 1), binds to a portion of the NMDA receptor and acts as a "cell death signal" during strokes.
Researchers hypothesized that by preventing DAPK1 from binding with the NMDA receptors, they could prevent the calcium overloads and cell deaths. They developed a potent compound to test their theory and found that the compound blocked DAPK1, protecting brain cells against stroke injury, and did not affect the beneficial physiological functions of the receptors.
"It is conceivable that this study not only provides new insights into the cellular and molecular basis responsible for stroke damage, but also provides a therapeutic target for stroke therapy," said Youming Lu, the LSU professor who led the team of scientists.
The findings appear in the Jan. 22 issue of Cell. (ANI)
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