This model has been reinforced by the fact that AP, CAA and NFT are also present in familial AD (FAD) due to presenilin (PS) and amyloid-β precursor protein (AβPP) mutations and are recapitulated in genetically-engineered transgenic (Tg) mice bearing mutated forms of AβPP, PS and tau. This evidence concerns the gene APP and alkaline phosphatase measurement.