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Neuroprotective Strategies for the Treatment of Blast-Induced Optic Neuropathy

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Technical Report,15 Sep 2015,14 Sep 2019

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Vanderbilt University Medical Center Nashville United States

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Background Over 186,000 eye injuries were diagnosed in fixed not deployed U.S. Military medical facilities from 2000-2011. We have a mouse model of blast trauma that causes vision loss and optic nerve degeneration secondary to blast-induced oxidative stress and neuroinflammation. Importantly, all of these processes also occur in other models of CNS trauma. Therefore, our study has implications for neurodegenerations from trauma extending beyond optic neuropathy. Objective To test the efficacy of targeted delivery of neuroprotective therapeutics in preventing degeneration of the retina and optic projection to the brain secondary to blast trauma. Galantamine was chosen because it preserves cholinergic signaling and is FDA approved for the treatment of Alzheimers disease. Erythropoietin EPO was chosen because it decreases both oxidative stress and neuroinflammation. We will use a modified form of EPOEPO-R76E that has attenuated erythropoietic activity and therefore is safer for clinical use. We will also examine the mechanisms underlying blast-induced vision loss with the goal of identifying additional drug targets for therapeutic intervention. We hypothesize that the vision loss and optic nerve degeneration that occurs after blast is due to oxidative stress and neuroinflammation. Military Benefit Currently there are no vision-preserving treatments available for trauma patients regardless of the mechanism of injury. Our study will determine the therapeutic efficacy of two FDA- approved neuroprotective agents.

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  • Medicine and Medical Research

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