The milestones in favor of this theory include genetic issues mainly provided by the discovery of pathogenic and protective mutations in the Amyloid Precursor Protein (APP; Selkoe, 1997; Di Fede et al., 2009; Jonsson et al., 2012; Hartley et al., 2015) and presenilin genes (Selkoe and Hardy, 2016), and the existence of polymorphisms in ApoE and other recently discovered genes modulating the risk of developing AD (Liao et al., 2017; Kunkle et al., 2019). This evidence concerns the gene APP and Alzheimer disease.