Mutations in these genes lead to pathogenic processing of APP to increase expression of Aβ 42 (Dai et al., 2017), a 42-residue-long fragment of APP which aggregates into Amyloid plaques in the brains of AD patients (Burdick et al., 1992; Gravina et al., 1995; Sun et al., 2015). This evidence concerns the gene APP and Alzheimer disease.