This study also has some strengths. A key strength is that this is a large and comprehensive exploration of PD GWAS and eQTL data sets from the human brain. We replicated our Coloc results across 2 platforms, Braineac and GTEx, generated through microarray and RNA-seq, respectively, and performed additional validation using TWAS in the CommonMind Consortium dorsolateral prefrontal cortex data set. This has resulted in prioritizing 11 candidate causal genes for PD based on GWAS results to be further investigated biologically in different animal or cell models for PD. Furthermore, we are highlighting biological reasons for their likely functional association with PD pathogenesis. We acknowledge that further functional work will be required to mechanistically link these genes to PD, but the genetic and analytical approaches applied here suggest that these are the putative gene and genomic events underlying these risk loci.
