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Animal model of Parkinson's disease reveals striking sensitivity to common environmental toxins

In findings that support a relationship between agricultural chemicals and Parkinson's disease, two groups of researchers have found new evidence that loss of DJ-1, a gene known to be linked to inherited Parkinson's disease, leads to striking sensitivity to the herbicide paraquat and the insecticide rotenone. The two studies were performed with the fruit fly Drosophila, a widely used model organism for studies of human disease, and shed new light on biological connections between inherited and sporadic forms of Parkinson's disease.

The work is reported in Current Biology by two independent groups, one led by Nancy Bonini of the University of Pennsylvania and the Howard Hughes Medical Institute, and the other led by Kyung-Tai Min of the NINDS branch of the U.S. National Institutes of Health.

Parkinson's disease occurs both sporadically and as a result of inheritance of single gene mutations. One of the most common neurodegenerative disorders, it is associated with the progressive and selective loss of a specific population of neurons in the brain, the dopaminergic neurons of the substantia nigra pars compacta . Exposure to several common environmental toxins, thought to injure neurons through oxidative damage, has been shown to be associated with sporadic forms of Parkinson's disease. During the past decade, researchers have also made remarkable progress in identifying genes responsible for inherited forms of Parkinson's disease, with the expectation that understanding the function of these genes will elucidate mechanisms behind sporadic Parkinson's disease. Past work had shown that one form of familial Parkinson's disease results from a loss of function of a gene called DJ-1.

The fruit fly possesses two versions of the DJ-1 gene, and in the new work, the researchers simulated the human Parkinson's disease situation by deleting one or both forms of DJ-1 from the fly's DNA.

Bonini and colleagues showed that flies lacking both forms
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Contact: Heidi Hardman
hhardman@cell.com
1-617-397-2879
Cell Press
6-Sep-2005


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