Abstract
Previous reports on Parkinson's disease indicate that genetic mutations in α-synuclein result in the aberrant accumulation of this protein, causing toxic gain of function leading to the development of Parkinson's. A recent report on the Iowan kindred, an extended pedigree with an autosomal dominant form of this disease, provides new mechanistic insight into Parkinson's disease by showing that an elevation in wild-type α-synuclein protein is sufficient to develop the early-onset form of the disorder. This review discusses how insights gained from these studies of α-synuclein may direct future research into Parkinson's disease.