A few cases have Mendelian inheritance trends, which often result in the early onset of symptoms through altered metabolism of Aβ,7 but for most patients, the genetic predisposition is more complex.8 The most common genetic risk factor is variants of the APOE gene,9 which is believed to mainly increase the risk for AD through modulating the accumulation of Aβ.10 In addition, genome-wide association studies (GWASs) have identified additional single-nucleotide polymorphisms (SNPs) with risk effects for AD dementia. Here, APOE is linked to Alzheimer disease.