With the increasing number of GWASs, our ability to map disease-associated variants exceeds our ability to interpret their biological function. Here, we have performed a comprehensive analysis by colocalization of eQTL and GWAS signals in PD, using a recent PD GWAS. We have integrated these data with publicly available brain eQTL data sets (Braineac and GTEx). This multilayered approach has identified 11 genes that we postulate underlie PD risk. Of these, 5 are associated with gene expression regulation, and 6 are associated with alternative splicing. We found evidence of methylation regulation for 3 of these candidate genes.
