ATLANTA--The irreversible neurological degeneration associated with Parkinson's and Alzheimer's diseases may be the consequence of oxidative stress--the imbalance of antioxidants and pro-oxidants in cells. This imbalance results in an excess of reactive oxygen species--harmful oxygen-containing molecules that can cause damage to proteins. In the April 21 issue of the Journal of Biological Chemistry, scientists from the Emory University School of Medicine report that the protein DJ-1 is oxidatively damaged in non-hereditary (sporadic) Parkinson's disease.

While scientists do not know the function of DJ-1, they have previously identified abnormalities in DJ-1 that directly cause hereditary (familial) Parkinson's disease. About 10 percent of Parkinson's disease cases are hereditary forms caused by either a genetic deletion or mutations that result in amino acid substitutions, which can dramatically affect protein structure or function.

The cause of the 90 percent of Parkinson's Disease cases not influenced by genetics has remained more of a mystery. Lian Li, PhD, is associate professor of pharmacology at Emory University School of Medicine and lead author of this study, which was funded by a grant from the National Institutes of Health. "One popular theory has suggested that these sporadic cases result from exposure to environmental toxins, such as herbicides or pesticides," she says. "Previous research has indicated that these toxins lead to oxidative stress. While oxidative stress does occur naturally as humans age, further oxidation caused by toxins may overwhelm the bodys antioxidants."

Until now, attempts to link environmental toxins to oxidation and neurological disorders have been only somewhat successful, in part because scientists have been unable to identify the molecular target of oxidation. "This theory [that toxins cause oxidative stress] has been around for a long time," says Dr. Li. "But whats been damaged by this oxida
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Contact: Holly Korschun
hkorsch@emory.edu
404-727-3990
Emory University Health Sciences Center
27-Apr-2006

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