Amyloid Neurotoxicity in Experimental Mouse Glaucoma

Stuart McKinnon, MD, PhD
Duke University (Durham, NC)
Year Awarded:
Grant Duration:
July 1, 2003 to June 30, 2005
Award Amount:
Grant Reference ID:
Award Type:
Award Region:
US Southern

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 Alxheimer'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.


1) McKinnon SJ. Glaucoma: Ocular Alzheimer's Disease? Front Biosci 2003; 8:s1140-56.  

2) Mayo GL, Melendez RF, Kumar N, McKinnon SJ, Glickman RD. Antibody-targeted photodynamic therapy. Am J Ophthalmol 2003; 136:1151-2.  

3) Tahzib NG, Reitsamer HA, Ransom NL, McKinnon SJ. Alpha-fodrin is cleaved by caspase-3 in a chronic ocular hypertensive (COH) rat model of glaucoma. Brain Res Bull 2004; 62:491-5.  

4) Reitsamer HA, Kiel JW, Harrison JM, Ransom NL, McKinnon SJ. Tonopen measurements of intraocular pressure in mice. Exp Eye Res 2004; 78:799-804.  

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