Notably, Aβo isolated from soluble fractions of AD human brain extracts, from mouse or cellular models of the disease or derived from synthetic preparations, have been shown to be bioactive and to consistently inhibit long‐term potentiation (LTP), an electrophysiological correlate of learning and memory (Lambert et al., 1998; Shankar et al., 2008; Walsh et al., 2002). Here, ABO is linked to Alzheimer disease.