Amyloid Neurotoxicity in Experimental Mouse Glaucoma

Dr. McKinnon’s hypothesis is that abnormal processing of the amyloid precursor protein (APP) and amyloid beta toxicity are important in the pathophysiology of glaucoma. He and his team are exploring the molecular events in glaucoma that mimic Alzheimer’s disease—i.e., those involving apoptosis and the abnormal processing of APP. Through the use of transgenic mouse lines, they will examine the over- or under-expression of Alzheimer’s-related proteins in both normal mice and mice that have been engineered to exhibit chronic ocular hypertension. In this way, he hopes to identify the critical steps that are operative in the death of retinal ganglion cells in glaucoma. The goal of this study is to identify new treatment strategies that might be used to treat not only glaucoma, but other neurodegenerative diseases as well.