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Alzheimer's disease as a case of brake failure?
Date:6/24/2008

l cycle, driving it forward through its various phases. The scientists focused on one particular kinase Cdk5 termed "an atypical kinase" because they could find no involvement in propelling the cell cycle. They found that while it appears to be inert as a cell cycle promoter, Cdk5 in the nervous system actually functions to hold the cell cycle in check.

"Its mere presence helps protect the brain," Herrup said. "What we discovered is that Cdk5 acts as a brake, not a driver."

Their latest laboratory research examined the workings of Cdk5 in human AD tissues and in a mouse model. Normally, the protein resides in the nerve cell nucleus, but in the presence of AD both in the mouse model and in the human tissue the disease process drives the protein out into the cell's cytoplasm. This disrupts the status quo, overrides the brake and unleashes a chain of events that ultimately leads to the death of the cells and the resulting dementia.

"The ejection of Cdk5 out of the nucleus is probably related to the changed chemistry of the Alzheimer's brain and chronic inflammation that accompanies AD," Herrup said.


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Contact: Joseph Blumberg
blumberg@ur.rutgers.edu
732-932-7084 x652
Rutgers University
Source:Eurekalert

Page: 1 2

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