Amyloid-β (Aβ) peptides cleaved from amyloid precursor protein (APP) are the key molecules involved in AD pathogenesis; deposition of Aβ in the brain as senile plaques and cerebral amyloid angiopathy (CAA) likely triggers a cascade of events leading to disease onset (Hardy and Selkoe, 2002; Blennow et al., 2006). This evidence concerns the gene APP and Senile plaques.