Dr. Warren J. Strittmatter was appointed as Chief of the Division of Neurology at Duke University Medical Center in October, 1998 and he holds the rank of Professor in the Departments of Medicine and Neurobiology. Dr. Strittmatter obtained his M.D. degree from Duke University School of Medicine in 1973. He then completed his internship at Emory-Grady Hospital, and returned to Duke as a Neurology Resident. Upon completing his residency in 1977, Dr. Strittmatter joined the Pharmacology-Toxicology Program at NIH as a Research Associate. In 1979 he went to Baylor College of Medicine as an Assistant Professor in the Departments of Neurology and Biochemistry. There, he rose through the ranks, being appointed as Professor and Co-Director of the Alzheimer’s Disease Research Center. In 1991 he returned to Duke’s Division of Neurology. In 1995, he was appointed as the Director of the Deane Laboratory to develop innovative basic and translational research in neurologic diseases. Under Dr. Strittmatter’s leadership, the Deane Laboratory’s objective is to expedite the drug-discovery process by identifying molecular targets and by developing novel molecular screening technologies. Dr. Strittmatter’s clinical and research activities focus on Alzheimer’s Disease and the CAG–triplet repeat diseases.

James O. McNamara, Sr. M.D.
Carl R. Deane Professor of Neuroscience, Division of Neurology

Dr. McNamara is the Carl R. Deane Professor of Neuroscience in the Departments of Medicine (Neurology), Neurobiology and Pharmacology at Duke University Medical Center. He is the Director of the Duke Center for the Advanced Study of Epilepsy and an attending neurologist at the Durham VA Medical Center. Dr. McNamara received his AB in Philosophy from Marquette University in 1964, and his MD from the University of Michigan School of Medicine in 1968. He completed his neurology training at the University of Michigan and Duke University. Following a postdoctoral fellowship in membrane biochemistry with Dr. Stanley Appel at Duke, Dr. McNamara joined the faculty at Duke. In 1990-91 he spent a sabbatical leave studying molecular neuroscience with Dr. Steve Heinemann at the Salk Institute.

Dr. McNamara’s research is centered on mechanisms of epileptogenesis. One line of investigation seeks to understand the molecular mechanisms by which pathologic activity leads to abnormal synapses in the mature mammalian nervous system. A second line of investigation centers on the role of humoral auto-immune responses to glutamate receptors in the pathogenesis of a human epilepsy, Rasmussen’s encephalitis.

Dr. McNamara was a member of the Neurology A Study Section at the National Institutes of Health from 1984-87 and currently serves on the Klingenstein Neuroscience Advisory Committee and the Board of Scientific Counselors of the National Institute of Neurological Disease and Stroke, NIH. He has received numerous awards for his research. He is the recipient of two consecutive Javits Neuroscience Investigator Awards from the National Institutes of Health, the Epilepsy Research Award from the American Society of Pharmacology and Experimental Therapeutics, and the Research Recognition Award, Basic Scientist, from the American Epilepsy Society, among others.

Dr. Burke is an Assistant Professor in the Division of Neurology at the Duke University School of Medicine. He received his undergraduate degree in Biology and English from Manhattan College. He graduated from the University of Tennessee-Oak Ridge National Laboratory Graduate School of Biomedical Sciences with a Ph.D. degree in Biochemistry. His thesis examined the effect of aging on the fidelity of protein synthesis.

Dr. Burke attended medical school at the State University of New York Health Sciences Center in Brooklyn and received his M.D. degree in 1985. Following an internship in New York, he completed a neurology residency and Aging fellowship at Duke University. Upon completion of his fellowship in 1993, Dr. Burke joined the faculty at Duke University Medical Center as an Assistant Professor. His clinical practice consists primarily of patients with neurodegenerative disease. He is the Director of Clinical Research on Dementia at the Joseph and Kathleen Bryan Alzheimer’s Disease Research Center.

The goal of Dr. Burke’s research is to understand the role of abnormal protein-protein interactions in the development of neurodegenerative disease. His laboratory studies polyglutamine as a model protein to characterize these interactions. He has received funding for this work from the Hereditary Disease Foundation and a Clinical Investigator Development Award from the National Institute of Neurologic Disorders and Stroke.

Burton Scott is an Associate in the Division of Neurology at Duke University Medical Center. He received his Ph.D. in Anatomy from Duke University, his M.D. from the University of Miami School of Medicine, and completed his residency training in Neurology at Duke. He received fellowship training in Movement Disorders with Dr. Joseph Jankovic in Houston, Texas, and joined the Duke Neurology faculty in 1995. Dr. Scott has a special interest in movement disorders, particularly Parkinson’s disease, and sees many patients referred to Duke for evaluation and treatment of Parkinson’s disease.

Dr. Scott’s research interests include exploring the role of a protein named a -synclein in causing a Parkinson’s disease-like illness. The biologic function of a -synuclein is not known, however, it is known that the protein accumulates within Lewy Bodies, the defining pathologic structures found in degenerating dopamine-containing nerve cells in the substantia nigra of patients affected with Parkinson’s disease. Mutations of the gene coding for a -synuclein have been associated with development of Parkinson’s symptoms in several members of a small number of families. Dr. Scott is studying protein-protein interactions between normal a -synuclein and other brain proteins, and is comparing these interactions with those observed between mutant a -synucleins and the same brain proteins. It is anticipated that a better understanding of the role of a -synuclein in families with Parkinson’s disease may shed light on disease mechanisms in the more common sporadic Parkinson’s disease, which afflicts up to 1 million patients in the United States alone.