Kos et al. (2013) were the first to examine the polygenic architecture of AD in both EA and AA populations. In their risk profile scoring analysis, the discovery sample consisted of 1,274 EA and 285 AA subjects from COGA, and the target sample consisted of 1,573 EA and 841 AA subjects from SAGE. GWAS was performed in the discovery sample and the results were LD pruned and binned according to P-value and minor allele frequency (MAF). Risk prediction scores derived from GWAS results in the discovery sample significantly predicted case-control status in both the EA and AA target samples, although the maximum variance explained in EAs (at a P-value threshold of 0.05) was only 0.73% (P=1.64 × 10−3) and in AAs (at a threshold of < 0.3) it was 2.14% (P=2.08 × 10−4). When binned by MAF, SNPs with higher allele frequencies explained more variance, with a peak of 0.3–0.4% in both populations (EA: 0.57%, P=0.0047; AA: 2.13%, P=1.3 × 10−4).
