Multiple genetic and environmental etiologies have been implicated in the pathogenesis of idiopathic Parkinson disease. Recent observations have suggested an association between chronic exposure to trichloroethylene (TCE) and development of clinical parkinsonism. Animal models of TCE exposure have shown nigrostriatal degeneration and the development of parkinsonian features. Animal and cell culture models indicate mitochondrial dysfunction as the probable mechanism, most likely mediated by TaClo, a potential TCE metabolite. These observations endorse the hypothesis that a variety of environmental risk factors may cause nigrostriatal degeneration and clinical parkinsonism in genetically predisposed individuals.
Published by Elsevier Inc.