1932

Abstract

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
Loading

Article metrics loading...

/content/journals/10.1146/annurev-genom-082410-101440
2011-06-02
2024-04-23
Loading full text...

Full text loading...

/content/journals/10.1146/annurev-genom-082410-101440
Loading
/content/journals/10.1146/annurev-genom-082410-101440
Loading

Data & Media loading...

  • Article Type: Review Article
This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error