Using florbetapir PET and GWAS, this study confirmed the association of APOE and identified a novel and independent association of BCHE to cerebral Aβ deposition. Together, the risk variants at these loci explained 15% of the variation in cortical Aβ levels, a substantial effect for two genes in a study of complex disease of this size. Additional loci, including both new genes and others previously studied in relation to AD, also displayed suggestive association to Aβ burden and provide further targets for follow-up.
