LOAD risk loci may also contribute to variation in age of onset (AAO) of LOAD, as do the allelic variants in APOE, however roles in AAO for the other newly identified risk loci (CLU, BIN1, and others) have not been explored. We examined variants at ten confirmed LOAD risk loci (APOE, CLU, PICALM, CR1, BIN1, CD2AP, EPHA1, the MS4A region, ABCA7, and CD33) to determine if they contribute to variation in AAO among 9,160 LOAD cases in the Alzheimer's disease Genetics Consortium (ADGC). We tested association with AAO for each locus using linear modeling with covariate adjustment for population substructure and performed a random-effects meta-analysis across datasets. We also examined genetic burden using genotype scores weighted by risk effect sizes to examine the aggregate contribution of these loci to variation in AAO. Analyses confirmed association of APOE regional variation with AAO (rs6857, P =3.30×10 -96), with statistically significant associations with AAO (P<0.005) demonstrated at several other LOAD risk loci, including rs6701713 in CR1 (P =0.00717), rs7561528 in BIN1 (P =0.00478), rs561655 in PICALM (P =0.00223). Associations remained largely unchanged after additional adjustment for dosage of APOE ε4 alleles. Burden analyses showed APOE contributes to 3.1% of variation in AAO (R 2 =0.078) whereas the other nine genes contribute to 1.1% of variation (R 2 =0.058) over baseline (R 2 =0.047). Secondary analyses of genome-wide association with AAO among non-risk loci identified several regions with multiple SNPs demonstrating suggestive associations (P<10 -6), including one nearing genome-wide statistical significance: MYO16 (47 SNPs; most significant: rs9521011, P =7.62×10 -8), CDH20 (4 SNPs; most significant: rs12956834, P =6.17×10 -6), and SGCZ (10 SNPs; most significant: rs7016159, P =7.70×10 -6). We confirmed the association of APOE variants with AAO among LOAD cases, and observe associations with AAO in CR1, BIN1, and PICALM. In contrast to earlier hypothetical modeling, we show that the combined effects of other loci do not exceed the effect of APOE on AAO, and if additional genetic contributions to AAO exist, they are likely very small individually or are hidden in gene-gene interactions.