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. Author manuscript; available in PMC: 2021 Jul 28.
Published in final edited form as: Nat Genet. 2021 Jan 28;53(2):143–146. doi: 10.1038/s41588-020-00773-z

Table 2:

COLOC and SMR analysis of the 13 significant genes in the discovery AD PWAS. Eleven genes had evidence consistent with a causal role by either COLOC or SMR.

COLOC SMR

Gene Chr H4 Causal variant SMR.p HEIDI.p Causal variant
1 CTSH 15 0.962 yes 3.1×10−5 0.464 yes
2 DOC2A 16 0.907 yes 1.0×10−3 0.742 yes
3 ICA1L 2 0.672 yes 4.1×10−4 0.977 yes
4 LACTB 15 0.754 yes 3.8×10−4 0.070 yes
5 PLEKHA1* 10 0.581 yes 3.0×10−3 0.455 yes
6 SNX32 11 0.975 yes 2.7×10−5 0.588 yes
7 STX4* 16 0.918 yes 5.0×10−3 0.808 yes
8 ACE 17 0.976 yes 4.0×10−3 0.039 no
9 RTFDC1 20 0.643 yes 4.6×10−5 0.034 no
10 CARHSP1 16 0.188 no 1.2×10−2 0.397 yes
11 STX6 1 0.072 no 1.0×10−2 0.748 yes
12 EPHX2 8 0 no 7.1×10−7 0.008 no
13 PVR* 19 0.022 no 1.4×10−5 n/a n/a

For the 13 FDR-significant genes in the discovery AD PWAS, the result of COLOC H4, which is the Bayesian posterior probability that a genetic variant is shared by both traits (i.e., gene and AD), and P values for SMR and SMR HEIDI tests are given.

(*)

Asterisk denotes genes not found in the confirmatory PWAS. n/a (not applicable) indicates undetermined result since the number of pQTL SNPs were too small for HEIDI to test. Genes were sorted by whether they are consistent with being a causal variant.