Alzheimer’s Disease (AD), the most common form of dementia, is the sixth leading cause of death in the United States. With a prevalence of over five million cases, the number of AD patients is expected to increase as a new diagnosis of AD is made every sixty-six seconds. Early symptoms include short-term memory loss and gradually progress to devastating deficits in cognition, temperament, and behavior. AD is a neurodegenerative disease linked to the accumulation and aggregation of two proteins, Aβ1-42 and hyperphosphorylated Tau, which form the characteristic amyloid plaques and neurofibrillary tangles found in the brains of AD patients. Previous studies support the notion that genetic variation underlies the wide array of phenotypes observed among AD patients, and several genes have been discovered to cause early onset AD. In sporadic (late onset) AD patients, it remains unknown what effects natural variation may have on the expression and severity of the AD phenotype. To explore the influence of genes on AD, our study utilizes a Drosophila model of AD that allows us to express both the Aβ1-42 and Tau peptides in the fly eye. Expression of AD-related proteins in the eye leads to degradation of the hundreds of ommatidia that make up the fly eye. To quantify the extent of ommatidial degradation, we use a computer program, ImageJ, which measures the size and circularity of each ommatidium. To introduce natural variation, the AD fly is crossed with flies from the Drosophila Genetic Reference Panel (DGRP), consisting of 192 fully sequenced isogenic lines. By comparing the Aβ1-42 and Tau-induced degradation in each background, we can identify naturally occurring modifiers of the AD phenotype. We have already identified promising hits, which could eventually help in the development of novel targeted therapies.