The amyloid hypothesis states that amyloid plaques formed by aggregates of Aβ peptide generated by the proteolytic cleavages of APP are central to AD pathology.[1] APP belongs to a large family of type I membrane proteins with a large extracellular domain and a short cytoplasmic region derived by differential splicing of a single gene transript located on the long arm of chromosome 21. Here, APP is linked to Alzheimer disease.