The GWAS results did not indicate evidence of spurious inflation of association test statistics (λ = 1.00) due to population stratification or other confounding factors (Figure 1). Loci on two chromosomes exhibited genome-wide significant association (p < 5 × 10−8) to cortical Aβ levels (Figure 2). As expected, the peak association originated on chromosome 19 from rs429358 (p = 5.45 × 10−14), which codes for the APOE ε4 allele.7 While other SNPs within APOE and in the region of its adjacent genes APOC1, TOMM40, and PVRL2 also displayed significant association to cortical Aβ levels in the primary GWAS model (Figure 2 and Figure 3A), their association signals disappeared (p > 0.05) when APOE ε4 status (absence = 0, presence = 1) was included as a covariate.
