In the early 1990’s, APOE was identified by candidate gene association as a susceptibility gene for late-onset AD in no small part due to its unusually large effect size (Table 3). 27,32 In 2009, GWAS from two large consortia 33,34 implicated three novel loci and six additional loci were identified in 2011. 35,36 Full meta-analyses are keenly awaited, but the 10 loci identified to date account for ~20% of the total variation in risk or ~33% of the risk attributable to genetic effects, with the major contribution being from APOE. Note that the association of one gene identified by GWAS, CR1, might result from SV. 37
