Table 2 An overview of previously conducted GWASs for depression and AD used in this study

From: Depression symptom-specific genetic associations in clinically diagnosed and proxy case Alzheimer’s disease

Phenotype (original GWAS)

Excluded samples

Cases (% clinical)

Controls (% clinical)

Total

h2SNP (s.e.)

Depression GWAS

Broad depression (Howard et al.10)

23andMe

170,756 (25.3%)

329,443 (29.0%)

500,199

0.0798 (0.003)

Clinical depression (Wray et al.9)

UK Biobank; 23andMe

45,591 (100%)

97,674 (100%)

143,261

0.1012 (0.007)

Alzheimer’s disease GWAS

Clinical + proxy AD (Bellenguez et al.15 (Stage 1))

NA

85,934 (45.5%)

401,577 (14.0%)

487,511

0.0306 (0.003)

Clinical + proxy AD (Wightman et al.14)

23andMe

86,531 (46.1%)

676,386 (26.1%)

762,917

0.0237 (0.004)

Clinical + proxy AD (Jansen et al.13)

NA

71,880 (33.5%)

383,378 (14.4%)

455,258

0.0234 (0.003)

Proxy-only AD (Marioni et al.31)

IGAP

42,035 (0%)

272,243 (0%)

314,278

0.0165 (0.003)

Clinical-only AD (Wightman et al. (no UKB) (2021))

UK Biobank; 23andMe

39,918 (100%)

358,140 (29.1%)

398,058

0.0431 (0.008)

Clinical-only AD (Kunkle et al.12 (Stage 1))

NA

21,982 (100%)

41,944 (86.2%)

63,926

0.068 (0.011)

  1. Heritability estimates were calculated naïvely on the liability scale from these standardized summary statistics using LDSC, taking a population prevalence of 15% for depression and 5% for AD. NA, not applicable; h2SNP, SNP heritability.
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