A report published in the April 21, 2006 issue of the Journal of Biological Chemistry revealed the findings of Emory University School of Medicine researchers that a protein known as DJ-1, which, when mutated, results in hereditary Parkinson's disease, is also involved in nonhereditary (sporadic) Parkinson's disease when it becomes damaged by oxidative stress. Approximately 90 percent of Parkinson's disease cases are believed to be nonhereditary. "One popular theory has suggested that these sporadic cases result from exposure to environmental toxins, such as herbicides or pesticides," lead author and associate professor of pharmacology Lian Li, PhD, observed. "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 body's antioxidants. This theory has been around for a long time. But what's been damaged by this oxidative stress?"

Doctor Li's team examined DJ-1 oxidation levels in the brains of individuals with nonhereditary Parkinson's and Alzheimer's disease, and age-matched controls and found that the protein showed signs of oxidative damage in the brains of the diseased patients. As in hereditary Parkinson's, structural changes to the protein leads to its loss and degradation. "The protein unfolds and cannot function normally," Dr Li explained. "Not recognizing the unfamiliar shape, the protein is broken down by the cell. The end result is the same: you lose your protein. Any mutation or modification causing this protein to lose its function will then lead to neurodegeneration in Parkinson's disease."

Dr Li is researching the possibility that DJ-1 could function as an antioxidant, leaving the cell vulnerable to oxidative damage when the protein is mutated. Until drugs are developed that target DJ-1, Dr Li notes that green tea and vitamin C are good dietary sources of antioxidants.