Drosophila eye model to identify genetic modifiers of A42 mediated neurodegeneration. Michael T. Moran, Oorvashi Roy Puli, Meghana Tare, Amit Singh. University of Dayton, Biology Department, 300 College Park Dayton, OH 45469.

   The neurodegeneration that results from Alzheimers disease (AD) is caused by the improper cleavage of APP to form the polypeptide amyloid beta 42 (A42). Being hydrophobic, A42 clumps together forming plaques which in turn accumulate around the neurons of the brain causing many cellular disturbances and, eventually, neuronal death. The characteristically slow degeneration of neurons in AD has been accredited to this accumulation of A42 in the brain. However, the exact mechanisms of how and why this accumulation happens are not yet fully understood. Using the A42 misexpression model where we misexpress A42 in the differentiating neurons of the eye using GMR-Gal4 driver, we carried out a screen to look for downstream modifiers of the neurodegenerative phenotype of A42 accumulation. Here we present the results of the screen and further characterizations of genetic interactions of two genetic modifiers and their role in A42 mediated neurodegeneration in the Drosophila eye.