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The Washington Research Foundation Fellowship

Derek Nhan, Neurobiology & Biochemistry, 2012-13 WRFF

Derek Nhan

Derek Nhan's interest in therapies for neurological diseases began as a freshman in a neurobiology course and has flourished while performing research under the mentorship of Dr. Kyra Becker in the Department of Neurology. He has been intrigued with the opportunity to explore a novel research question and design targeted experiments that have the impact of improving clinical treatments for patients with medical disorders. In the Becker Lab, he has been involved in several projects associated with the consequences of post-stroke cerebrovascular damage and his most recent project focuses on the morphologies of neuronal damage as a marker for worse clinical outcome. With support from the WRF Fellowship, he hopes to develop a functional animal model to characterize post-stroke outcome at a cellular and behavioral level. Following graduation, Derek intends to pursue a career in biomedical research combining developments at the bench with the opportunity to deliver them to patients.

Mentor: Kyra Becker, Neurology

Project Title: Central Demyelination Following Ischemic Stroke in an Animal Model

Abstract: Over 800,000 Americans suffer a stroke each year, making this neurological disease the leading cause of long-term adult disability in the United States. An ischemic stroke occurs when blood flow to the brain is interrupted, resulting in inadequate oxygen delivery to brain cells. White matter, largely the myelin sheaths around axons, represents a prominent target of such hypoxic-ischemic injuries and effective interventions given post-stroke are sorely needed. This interaction becomes particularly exasperated in stroke patients due to the breakdown of the blood-brain barrier allowing for interactions between once-segregated central nervous system antigens and lymphocytes from the body. My project investigates the interactions between the autoimmune antigen, myelin basic protein- critical for the development of myelin- and its inflammatory effects on the central nervous system as a predictor of motor dysfunction in an animal model. We induced a stroke in Lewis rats using middle cerebral arterial occlusion and injected them with either lipopolysaccharhide, previously shown to elicit an immune response, or saline for control. I performed a battery of behavioral tests, including the standard neurological score and rotarod a week prior to induction of the stroke and for two and four weeks after. Using immunohistochemistry and luxol fast blue staining, the brains were labeled and a quantitative analysis of myelin coverage between the infracted and the non-infarcted hemispheres were performed using a semi-automated system called Metamorph. Preliminary data has shown demyelination present especially in the caudate-putamen region responsible for regulating movements and often associated with various types of learning behaviors. Additionally, we have observed a correlation between increased myelin loss and reduced motor function immediately post-stroke though further results are pending. These data are critical for developing an animal model for demyelination following ischemic stroke, necessary for characterization of myelin damage as a robust neural marker for mediating worse clinical outcome.