Mutations in PS1 or PS2 can affect the degradation and transport of APP, increase Aβ42 production and the Aβ42/Aβ40 ratio, and affect the interaction between tau protein and other cytoskeletal proteins, thereby attributing to the pathogenesis of AD (Kumar-Singh et al., 2006; Campion et al., 2016; Eggert et al., 2018). This evidence concerns the gene APP and Alzheimer disease.