Genetic studies have provided valuable insight into the pathological mechanisms underlying Parkinson's disease (PD). The elucidation of genetic components to what was once largely considered a nongenetic disease has given rise to a multitude of cell and animal models enabling the dissection of molecular pathways involved in disease etiology. Here, we review advances obtained from models of dominant mutations in and as well as recessive , and mutations. Recent genome-wide association studies have implicated genetic variability at two of these loci, and , as significant risk factors for developing sporadic PD. This, coupled with the established role of mitochondrial impairment in both familial and sporadic PD, highlights the likelihood of common mechanisms fundamental to the etiology of both.

Keyword(s): DJ-1LRRK2PARISparkinPINK1α-synuclein

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  • Article Type: Review Article
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