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Blocking cell suicide switch fails to stop prion damage in mouse brains

St. Louis, Dec. 21, 2004 -- Researchers knew that prions, the misfolded proteins that cause mad cow disease and other brain disorders, were killing off a class of important brain cells in a transgenic mouse model. But when they found a way to rescue those cells, they were astonished to discover the mice still became sick.

Now they believe previous efforts to find the beginnings of the mouse disorder may have been focused on the wrong part of the brain cell and are plotting new directions for research.

In a study that appears in the Jan. 1 issue of the Proceedings of the National Academy of Sciences, scientists report evidence that clinical symptoms in the mice are produced by damage to synapses, the areas where nerve cell branches come together for communication.

"This could have important therapeutic implications," says senior author David Harris, M.D, Ph.D, professor of cell biology and physiology at Washington University School of Medicine in St. Louis. "There's a great deal of effort being put into developing treatments for neurodegenerative disorders that would inhibit neuron death. Our results suggest that if we just prevent cell death without doing something to maintain the functionality of the synapse, patients may still get sick."

Harris notes that the findings also link prion diseases, which are relatively rare, to more common neurodegenerative disorders like Alzheimer's disease, where recent evidence has also elevated the importance of damage to synapses.

Because of the bizarre methods by which prions spread and cause disease, they have only recently gained widespread acceptance as the source of several disorders that rapidly devastate the brains of humans, cows, deer and sheep.

In these disorders, the most infamous of which is mad cow disease, copies of a normal brain protein, PrP, fold themselves into abnormal shapes, dramatically altering the proteins' properties. Genetic mutations can increase ch
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Contact: Michael C. Purdy
purdym@wustl.edu
314-286-0122
Washington University School of Medicine
21-Dec-2004


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