Invited Speakers

Parkinson’s Disease, Environment and Genes
August 25 - 28, 2001 l Doubletree Hotel World Arena l Colorado Springs, Colorado

Flint M. Beal, Cornell University. His basic research work has provided the rationale for several clinical trials testing the effects of antioxidants in Parkinson’s disease.

Deborah A. Cory-Slechta (Conference Co-Chair), University of Rochester. Recently published work indicating that combined exposure to paraquat and maneb damages the mouse nigrostriatal system.

Mahlon R. DeLong, Emory University. One of the leading experts in surgical procedures such as pallidotomy and deep brain stimulation.

Donato A. Di Monte (Conference Co-Chair), The Parkinson’s Institute. Carrying out studies on the pathologic effects and mechanisms of interactions between a-synuclein and environmental agents.

Anthony L. Fink, University of California - Santa Cruz. Expert in mechanisms of protein aggregation and its potential role in neurodegenerative processes.

Lysia S. Forno, Stanford University and Palo Alto VA Hospital. World-recognized neuropathologist with over 50-years experience in human neurodegenerative processes and animal models of nigrostriatal damage.

J. Timothy Greenamyre, Emory University. Recently developed a novel rat model of Parkinson’s disease based on chronic inhibition of complex I by the pesticide rotenone.

Richard H. Haas, University of California - San Diego. His research group has been working on the role of coenzyme Q and mitochondrial electron transport defects in Parkinson’s disease.

John A. Hardy, Mayo Clinic at Jacksonville. Conducting several studies on familial cases of Parkinson’s disease with the aim of identifying specific genetic risk factors.

Ole Isacson, Harvard University. Involved in experimental and clinical work on fetal and stem cell transplantations as therapeutic approaches in Parkinson’s disease.

J. William Langston, The Parkinson’s Institute. With his discovery of MPTP, he has played a major role in our understanding of the effects and mechanisms of action of neurotoxicants in relation to human parkinsonism.

Peter T. Lansbury, Harvard University. His studies on the mechanisms and consequences on a-synuclein oligomerization have direct implications on our understanding of its pathologic role in human parkinsonism.

Eliezer Masliah, University of California - San Diego. Described (in the journal Science) neuropathologic features resembling those of Parkinson’s disease in transgenic mice overexpressing a-synuclein.

Gary W. Miller, University of Texas Austin. Focused on the role of dopamine transporters and pesticides in Parkinson’s disease and has shown that organo- chlorine insecticides increase the expression of the plasma membrane dopamine transporter in the brains of mice treated with these compounds. Hypothesized that the increase in dopamine transporter expression represents one of the ways that pesticide exposure increases the incidence of Parkinson’s disease.

Lorene M. Nelson, Stanford University. Recently directed a large epidemiological study evaluating specific environmental and genetic risk factors for Parkinson’s disease.

Eric K. Richfield, University of Rochester. Involved with the establishment of an a-synuclein mouse model in which the human wild-type or a mutated form of the protein is expressed in catecholaminergic cell lines. His expertise is in both the neurochemistry and neuropathology of neurodegenerative diseases.

Caroline M. Tanner, The Parkinson’s Institute. Her work on Parkinson’s disease in twins has prompted a great debate on the respective roles of environmental and genetic risk factors in the past 2 years.

John Q. Trojanowski, University of Pennsylvania. He was the first to identify a-synuclein as a primary component of Lewy bodies and to hypothesize that protein aggregation may play a critical role in the pathogenesis of Parkinson’s disease.