Our estimates of measured contributions of the PRS to background heritability for Alzheimer’s disease risk, in the same sample, are smaller than the SNP-heritability estimates as well as that for APOE ɛ4.7–9 While the small contribution of the PRS in this study can potentially be explained by the fact that it is based on the most significant SNPs (N = 89),7 we note that including PRSs at more relaxed P-value thresholds did not pick up more heritability than SNPs with P < 1 × 10−5. This evidence concerns the gene APOE and early-onset autosomal dominant Alzheimer disease.