We present a systematic interrogation of all known PD risk loci using a recent PD GWAS, the aforementioned data sets, and methods to uncover the genes and mechanisms through which GWAS risk variants are associated with PD risk. The candidate genes and resulting pathways presented in this study are the result of stringent replication across multiple data sets and bioinformatic methods. We anticipate that this work can serve as a reference example to be applied to different neurodegenerative diseases.
