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Scientists Find New Trigger For Nerve Cell Death

St. Louis, Oct. 3, 1997 -- A paper in today's Science challenges a well-established idea about why nerve cells self-destruct when the brain or spinal cord is injured or becomes diseased. It suggests that when potassium jumps ship, neurons commit suicide.

"If our hypothesis proves correct, it will open up new possibilities for protecting nerve cells in patients who suffer stroke, head injury, spinal cord injury or neurodegenerative disorders such as Alzheimer's disease," says Dennis W. Choi, M.D., Ph.D., the Jones Professor and head of neurology at Washington University School of Medicine in St. Louis.

Choi, who directs the Center for the Study of Nervous System Injury, was the senior investigator in the study. The novel idea was the brainchild of lead author Shan Ping Yu, M.D., Ph.D., research assistant professor of neurology.

In the hours or days after the brain is injured, healthy cells surrounding the damaged region also die, killing themselves through a genetically controlled process called programmed cell death or apoptosis. Scientists previously have focused attention on changes in the amount of calcium contained within cells undergoing apoptosis. But Yu's experiments suggest that a mass exodus of potassium may be just as important as changes in calcium.

Potassium ions cross the cell membrane through tunnels called potassium channels, which control the rate at which they flow. If these channels play a key role in apoptosis, it might be possible to use drugs called potassium channel blockers to stem potassium loss and prevent nerve cells from dying. This might restrict damage to the initially injured area of the brain or spinal cord, allowing patients to recover more fully.

Yu got his idea by considering how apoptotic cells differ from those in the throes of necrosis -- sudden death at the focus of an injury. Whereas necrotic cells swell up and burst, apoptotic cells shrink into oblivion. "
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Contact: Linda Sage
sage@medicine.WUSTL.edu
314-286-0119
Washington University School of Medicine
3-Oct-1997


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