Funded Studies
Parkinson's disease results from a loss of dopamine neurons in brain areas that control body movement. However, the cause of this loss is unknown and thus it has been difficult to develop rational strategies to eliminate the disorder. Recently it was discovered that mutations in the gene for alpha-synuclein are associated with some cases of familial Parkinson's disease. Thus, alpha-synuclein may provide clues regarding the pathogenesis of this disease. We have developed cellular models to study the effects of alterations in alpha-synuclein and the mechanisms by which trophic factors can rescue dopamine neurons from toxic insults. Using these models, we will explore the hypothesis that normal levels of alpha-synuclein expression increase the capacity of dopamine neurons to resist the neurotoxic effects of a variety of agents, whereas reduced levels of alpha-synuclein or mutant alpha-synuclein increases neuronal vulnerability. We then will explore the ability of glial cell line derived neurotrophic factor (GDNF) to protect dopamine neurons against the cell death associated with alpha-synuclein abnormalities. We hope that these studies will help in the development of pharmacological strategies for protecting dopamine neurons from dying.
Michael J. Zigmond received his undergraduate degree in chemical engineering in 1963 from Carnegie Institute of Technology (now Carnegie Mellon University). He received a PhD from the University of Chicago in 1968. After postdoctoral training at the Massachusetts Institute of Technology, he joined the faculty of the University of Pittsburgh School of Medicine in 1970 and now serves there as a professor of neurology and psychiatry. Zigmond's research interests focus on the survival, death, and adaptation of neurons, particularly those that utilize dopamine and other catecholamines as neurotransmitters. In addition to his work at the National Parkinson Foundation Center of Excellence, he is associate director for basic research of the Pittsburgh Institute for Neurodegenerative Disease and directs a research program in basal ganglia and parkinsonism supported by the National Institute of Neurological Disorders and Stroke (NINDS). Zigmond was secretary for the 15,000-member Society for Neuroscience from 1994 to 1995 and is currently the editor in chief of Progress in Neurobiology.
Michael J. Zigmond received his undergraduate degree in chemical engineering in 1963 from Carnegie Institute of Technology (now Carnegie Mellon University). He received a PhD from the University of Chicago in 1968. After postdoctoral training at the Massachusetts Institute of Technology, he joined the faculty of the University of Pittsburgh School of Medicine in 1970 and now serves there as a professor of neurology and psychiatry. Zigmond's research interests focus on the survival, death, and adaptation of neurons, particularly those that utilize dopamine and other catecholamines as neurotransmitters. In addition to his work at the National Parkinson Foundation Center of Excellence, he is associate director for basic research of the Pittsburgh Institute for Neurodegenerative Disease and directs a research program in basal ganglia and parkinsonism supported by the National Institute of Neurological Disorders and Stroke (NINDS). Zigmond was secretary for the 15,000-member Society for Neuroscience from 1994 to 1995 and is currently the editor in chief of Progress in Neurobiology.