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Excerpt from the December 1996 Parkinson's Action Network "Action Reporter", an Advocacy Report for the Parkinson's Community- 1996 Has Been Landmark Year in Parkinson's Research >From basic research into the cause to clinical trials of new therapies, this was a landmark year in the quest to understand-and conquer-Parkinson's disease. Researchers have long noted that the disease appears more common in some families than others, so studying genetic factors is one way to determine the cause. Studies have also shown that environmental factors, possibly including infections or chemical exposure, play a role in most cases. A second 1996 study identifying genetic links with Parkinson's produced similar conclusions. In a report published in the October issue of the Annals of Neurology, a team of scientists from the University of Virginia and California-based biopharmaceutical company MitoKor have found a genetic defect that may contribute to the development of Parkinson's in some patients. The defect affects a mitochondrial enzyme called "Complex 1," an integral part of the energy generating mechanism of each cell. When comparing cell lines from Parkinson's patients with those of a non-Parkinson's control group, researchers observed that the Parkinson's cells exhibited 20% less Complex 1 activity than the control group. Additional tests determined that the Parkinson's cells also showed a greater susceptibility to MPTP, a toxin known to cause Parkinson's like symptoms. "The observation that a specific biochemical defect can render cells more vulnerable to MPTP toxicity illustrates how interactions between an environmental mitochondrial toxin and an apparent mitochondrial DNA defect could accelerate neuro-degeneration. This may explain why some individuals develop Parkinson's disease following toxin exposure, while others similarly subjected to the same toxin at the same dose do not," said Dr. Russell Swerdlow, U. Va. neurologist and lead author of the study. In commenting on this study, other Parkinson's researchers have expressed guarded optimism at the findings. "If confirmed by others, great support will be given to the idea that mitochondrial toxins, endogenous and exogenous, should be sought to help explain the etiology of Parkinson's disease," said Jay M. Gorell, M.D., Head of the Division of Movement Disorders in the Henry Ford Health System's Department of Neurology. "Remember though, that they have not excluded a faulty nuclear DNA contribution to mitochondrial Complex 1 function." If you have any questions or comments regarding the scientific research described here, please contact PAN at (800) 850-4726 Parkinson's Action Network 800-850-4726 Headquarters: 818 College Ave., Suite C Santa Rosa, CA 95404 phone 707-544-1994 fax 707-544-2363 email: [log in to unmask] Washington, DC office 601 13th St. NW., Suite 310 Washington, DC 20005 phone 202-628-2079 fax 202-628-2077 Brad Udall, Chair Joan I. Samuelson, President John L. Dodge, Treasurer Bonnie K. Mioduchoski, Administrator Michael Claeys, Community Coordinator The Action Reporter is a free publication of the Parkinson's Action Network, a non-profit charitable foundation for a cure for Parkinson's. Use of this material in other publications is welcomed. We ask that the Network be identified as the source of the material, and notified how, when and where the material is used. Simply call 800-850-4726