APP and Alzheimer disease: At present, Presenilin1 provide the catalytic protease activity that is independent and necessary for γ-secretase [22].The mutations and deletion of preseilin1 are reported to cause AD (especially in early-onset AD) through aberrant APP processing determining either increased Aβ levels or increased production of Aβ42 (and Aβ43) peptide rather than Aβ40, leading to Aβ aggregation [23].