Evidence relating to Aβ from autosomal dominant genetic mutations in the amyloid precursor protein (APP) and presenilins (PS) in familial AD (FAD) [9, 10], coupled with the neuropathological diagnostic value associated with the presence of deposits of Aβ in the brain in both FAD and sporadic AD (SAD) [11, 12], has been interpreted in the amyloid cascade hypothesis as showing a causal role for Aβ in disease progression [13, 14] and has been updated to reflect the ratios of Aβ (1–42)/Aβ (1–40) [14, 15] or oligomers [16, 17]. Here, APP is linked to familial Alzheimer disease.