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2006 Grant - Duff
p25/cdk5 in Alzheimer's Disease Pathogenesis
Karen Duff, Ph.D.
The Nathan S. Kline Institute for Psychiatric Research
Orangeburg, New York
2006 Zenith Fellows Award
One of the hallmarks of Alzheimer's disease pathology is the assembly of the beta-amyloid protein fragment into structures that appear to have a toxic effect on neurons. Although much is known about the identity and function of proteins immediately involved in the production of beta-amyloid, there are most likely other molecular events that precede, regulate and influence beta-amyloid-related proteins and their activities.
Karen Duff, Ph.D., and colleagues are investigating the work of a protein called p25, which activates a specialized protein called cdk5. Their studies have shown elevations of the p25/cdk5 pair are associated with an increase in beta-amyloid production. In this current work, the investigators will use cell cultures to exam the mechanisms by which p25/cdk5 contributes to this phenomenon.
They will focus on how p25/cdk5 may influence BACE, one of the proteins directly involved in beta-amyloid production. They hope to characterize how p25/cdk5 exerts its influence, what physiological consequences result from its influence, and how it may exacerbate Alzheimer's disease pathology. A better understanding of these earlier players and events may shed light on factors contributing to Alzheimer pathology and suggest new targets for drug development.