This study has some limitations. It considered only cis-QTLs, owing to the current challenges in robustly quantifying trans-QTLs. Furthermore, this study considered only QTLs in the brain and no other tissues. The Coloc analysis applied here assumes that the true causal variant underlying the disease has been captured in both the GWAS and eQTL data sets. The PD GWAS data used here have been imputed to the latest Haplotype Reference Consortium panel (version 1.1), and the genotypes in the GTEx data are generated with whole-genome sequencing, maximizing the chances of this assumption being met. However, the Braineac data used here have been imputed to 1000 Genomes phase 1, potentially reducing our power to replicate candidate genes in this data set. Another limitation in the colocalization tools used here is that they assume 1 independent signal for each gene at each locus for both the GWAS and QTL results. Finally, the methods used here cannot exclude pleiotropy, whereby a disease-causing SNV is associated with the regulation of an unrelated gene via a separate pathway.
