Aβ is an endogenous peptide that is cleaved from a larger transmembrane amyloid precursor protein (APP) by the action of the β‐secretase and γ‐secretase complex, which includes the presenilins, PS1 and PS2.[5] There is a large body of evidence to indicate that over production, increased aggregation, or reduced clearance of Aβ, is the key event in the pathology of AD.[6] A clear direct link between Aβ and AD is apparent for those with inherited early‐onset AD. This evidence concerns the gene APP and Alzheimer disease.