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

That's important by itself, because it tells us that Bax is involved in the cell death pathway," Harris notes. "There are other options for self-destruction that the cells could have been using, but now we know that the Bax pathway is the one to focus on."

Although the neurons survived, the clinical symptoms persisted. Microscopic examinations of the brains of mice from the original prion model had previously revealed clumps of prion protein in brain areas heavy with synapses, so researchers decided to look at the health of synapses in the new crossbred line of mice.

A test for synaptophysin, a protein found at synapses, revealed widespread loss of synapses in the new line of mice.

"The neurons were still alive, but their connections were damaged or missing," Harris says. "This discovery really has changed the way we think about future directions for our work."

According to Harris, future research will include studies of how prions damage the synapse and whether the clumps of prion protein are involved in that damage.


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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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