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2007 Grant - Bamji
Beta-Catenin Stabilization in the Synaptic Pathology of Alzheimer's Disease
Shernaz Xerxes Bamji, Ph.D.
University of British Columbia
Vancouver, British Columbia, Canada
2007 New Investigator Research Grant
Mutated forms of the protein presenilin-1 are strongly associated with the rare familial, or inherited, form of Alzheimer's disease. Though the reasons for this association are unclear, recent studies have found that presenilin-1 mutations may lead to abnormal levels of another protein called beta-catenin. Beta-catenin plays an important role in transmitting signals through a cell's interior, including messages that activate certain genes. However, people with familial Alzheimer's disease often have abnormally high levels of this protein in their brains. Scientists have found that normal presenilin-1 binds to beta-catenin, a process that destabilizes beta-catenin and targets it for destruction. Yet mutated presenilin-1 may lack the ability to carry out this important regulatory function.
Shernaz Xerxes Bamji, Ph.D., and colleagues hypothesize that presenilin-related increases in beta-catenin levels may hinder the ability of cells to communicate with one another in familial Alzheimer's disease. The researchers will test this hypothesis using both laboratory brain cells and mice genetically engineered to develop an Alzheimer-like pathology. They hope to learn more about how beta-catenin damages synapses, or specialized junctions through which cells transmit signals. Dr. Bamji and colleagues hope to analyze how such damage leads to brain cell death, brain dysfunction and cognitive loss in familial Alzheimer's. Results from this work could suggest novel approaches for future drug development.