Studies have shown that Aβ1–40 affects the activity of PKC, and Aβ1–40 degrades 70% of PKCγ isoforms in AD fibroblasts and 75% of PKCα in normal aged controls[47], while Aβ28–30 residues inhibit the phorbol-12,13-dibutyrate-induced membrane translocation of PKCα and PKCε without altering their expression levels[41]. This evidence concerns the gene PRKCA and Alzheimer disease.