Role of Kinesin-I and JIP1 in APP Trafficking
Kristen J. Verhey, PhD
University of Michigan
Ann Arbor, Michigan
2003 New Investigator Research Grant
A key feature of Alzheimer’s disease is the accumulation of beta-amyloid protein fragments in the brain. This fragment is clipped from its parent molecule, the amyloid precursor protein (APP). Although the normal tasks of APP are unclear, studies have suggested that it may have several responsibilities in essential cell functions. Because APP’s “partners” in its normal tasks may also be related to the abnormal breakdown of APP that produces beta-amyloid, scientists are interested in clarifying the interactions of APP with other proteins and structures in the cell.
In order for beta-amyloid production to occur, APP must be transported to the surface of the cell. Essentially, it is picked up like a piece of cargo and transported along a particular route. This research group is investigating two proteins, one that powers the delivery of APP and one that keeps it on its route. The researchers will study what molecular mechanisms make this process work and whether other players in beta-amyloid processing are transported in this same delivery system.
A better understanding of the transport, function, and processing of APP may suggest targets for developing therapies that inhibit the production of beta-amyloid.





