In total, 40 Alzheimer’s disease susceptibility loci reached genome–wide significance in at least one of the four GWAS we discuss (table 1). 15 were replicated across all four GWAS, and nine were significant in two or three studies. Two loci identified by the 2013 GWAS,5 three loci in the 2018 GWAX8 and 2019 GWAS,9 and eight in the 2019 GWAX7 were not replicated at full genome–wide significance in the other studies (table 1, figure). All but four of those loci (7q35, 16q23.3, 17q21.33, and 18q21.31) reached genome–wide suggestive significance (p<1 × 10−5) in at least one of these four studies, suggesting increased sample sizes improved statistical power to detect previous suggestive loci. The direction of effect was also consistent across studies after accounting for linkage disequilibrium in all except six loci (5q14.3, 6p21.1, 7p14.1, 16p12.3, 19p13.3, and 21q21.3), which are among those containing multiple independent variants. However, there was extensive overlap in the sample used between all four Alzheimer’s disease GWAS, so these studies are not independent. Across these 40 susceptibility loci, associations were reported for 78 unique lead SNPs—although
