| dbo:abstract |
Dennis W. Choi, M.D., Ph.D., was on the faculty of Stanford University in the 1980s, and served as the Jones Professor and Head of Neurology at Washington University in St. Louis during the 1990s, leaving in January 2001 to work in industry (Merck). While a faculty member at Washington University, Choi was a key contributor to research on glutamate-mediated toxicity ("excitotoxicity") as a mechanism of neural injury in stroke and traumatic brain injury. Choi attended Harvard College, from which he graduated in 1974, and went on to Harvard Medical School and the Harvard-MIT Division of Health Sciences and Technology to receive an MD and a PhD in Pharmacology in 1978. As a graduate student he demonstrated that benzodiazepines augment GABA-A receptor function, which represents a seminal discovery in neuroscience. Choi also completed his residency and fellowship in Neurology at Harvard. Choi joined Emory University in 2007, where he served as the Director of the Comprehensive Neurosciences Center and the Neuroscience, Human Nature, and Society Initiative. He was also a professor in the departments of neurology, pharmacology, and pediatrics. In the Spring of 2009, Choi taught an undergraduate course entitled "Neurofunction and Artificial Intelligence" for the Emory University Neuroscience & Behavioral Biology Program. He is currently the chair of the Department of Neurology at Stony Brook University School of Medicine in New York as well as Director of the Neurosciences Institute there. He sits on the scientific advisory boards of several companies and foundations, including the Cure Alzheimer's Fund. (en) |
| rdfs:comment |
Dennis W. Choi, M.D., Ph.D., was on the faculty of Stanford University in the 1980s, and served as the Jones Professor and Head of Neurology at Washington University in St. Louis during the 1990s, leaving in January 2001 to work in industry (Merck). While a faculty member at Washington University, Choi was a key contributor to research on glutamate-mediated toxicity ("excitotoxicity") as a mechanism of neural injury in stroke and traumatic brain injury. (en) |
