Of the candidate genes presented here, CD38 is associated with insulin regulation, emphasizing a possible role of glucose metabolism in PD.29 This finding is supported by recent work indicating an association between body mass index and PD, and a randomized clinical trial of exenatide, a glucagon-like peptide 1 receptor agonist, as a disease-modifying agent for PD.30,31 Furthermore, a role for CD38 in regulating neuroinflammation, especially in glial cells, has been proposed, which is consistent with the enrichment of CD38 in astrocytes in the cell-type specificity analysis.32 The data from this study also reinforce RAB29 as a key candidate for the chromosome 1q32 locus association. Recent studies providing further functional evidence linking RAB29 (also known as RAB7L1) to LRRK2, and implicating RAB29 as a substrate for LRRK2 kinase activity, also support this designation.33,34,35 Furthermore, the candidate genes CTSB and GALC, whose dysfunction is linked to lysosomal storage disorders such as Krabbe disease, are consistent with the findings on the role of lysosomal pathways in PD.36,37,38 In the GPNMB/NUPL2 locus, the PD GWAS results suggest only 1 independent signal, while the results
