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J. Timothy Greenamyre, MD, PhD - Scientific Advisory Board
Director, Pittsburgh Institute for Neurodegenerative Diseases
Chief, Division of Movement Disorders
University of Pittsburgh
Pittsburgh, Pennsylvania
Tim Greenamyre received his BS from Michigan State University and his MD and PhD from the University of Michigan. After his Neurology residency at the University of Michigan, he joined the faculty of the University of Rochester in 1990, and was recruited to Emory University in 1995. He moved to the University of Pittsburgh in 2005. He received the Roland B. Mackay Award (1986) and a Research Fellowship Award (1990-1993) from the American Academy of Neurology, and he was a Mallinckrodt Scholar (1994-1997). He chaired the Research Grants Subcommittee of the Huntington's Disease Society of America, and was a member of the NIH Parkinson's Disease Research Agenda Planning Committee, the Parkinson's Disease Implementation Committee and the Neurological Sciences and Disorders B Study Section of the NINDS. He is Chair of the Scientific Advisory Committee of the Parkinson Study Group, and a member of the Scientific Advisory Board of the Michael J. Fox Foundation, the Cure Parkinson's Project, the Parkinson's Disease Foundation, the Huntington's Disease Society of America, and Telethon Italy. He is Editor of Neurobiology of Disease, Associate Editor of The Journal of Neuroscience, and Section Editor for Functional Neurology, and he serves on the editorial boards of Neurology, Movement Disorders and Critical Reviews in Neurobiology. He has received several honors and in October 2004, he delivered a Presidential Lecture at the Annual Meeting of the Society for Neuroscience.
His lab is interested in mechanisms that cause nerve cell death in disorders such as Parkinson's, Huntington's and Alzheimer's diseases. With respect to Parkinson's disease, he is interested in interactions between environmental toxins (natural or man-made) and genes that increase or decrease an individual's susceptibility to developing the disease. The work focuses on mitochondrial impairment, oxidative damage and protein aggregation. The general strategy is to define mechanisms that cause nerve cell death, and then use them as potential "targets" for therapeutic intervention. The lab employs in vivo models of neurodegeneration and in vitro culture of cells and brain slices to study mechanisms of degeneration with a variety of biochemical, anatomical and physiological techniques. Another interest of the lab is the role of glutamate neurotransmission in the symptoms of Parkinson's disease.
Recent references:
Betarbet, R, Sherer, TB, MacKenzie, G, Garcia-Osuna, M, Panov, AV and Greenamyre, JT, Chronic systemic pesticide exposure reproduces features of Parkinson's disease, NatureeNeuroscience 3:1301-1306, 2000.
AV Panov, C-A Gutekunst, BR Leavitt, MR Hayden, JR Burke, WJ Strittmatter, JT Greenamyre, Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines, Nature Neuroscience 5:731-736, 2002.
Sherer TB, Betarbet R, Testa CM, Seo BB, Richardson JR, Kim J-H, Miller GW, Yagi T, Matsuno-Yagi A, and Greenamyre JT, Mechanism of toxicity in rotenone models of Parkinson's disease, J Neurosci 23:10756-10764, 2003.
Papa S, Auberson YP and Greenamyre JT, Prolongation of levodopa responses by glycineB antagonists in parkinsonian primates, Ann Neurol 56:723-727, 2004.
Greenamyre JT and Hastings TG, Parkinson's Divergent causes, convergent mechanisms. Science 304:1120-1122, 2004.
Greene JG, Dingledine R and Greenamyre JT, Gene expression profiling of rat midbrain dopamine neurons: implications for selective vulnerability in parkinsonism, Neurobiol Dis, 18:19-31, 2005.
