To support the role of BDNF in APP processing, both human (post‐mortem brains of patients with Alzheimer's disease (Allen et al., 1999; Ferrer et al., 2000; Fumagalli et al., 2006; Hock et al., 2000; Holsinger et al., 2000; Phillips et al., 1991)) and rodent models (APPNLh/PS‐1P264L and TgCRND8 (Peng et al., 2009)) in which Aβ accumulation occurs, display lower expression and protein content of BDNF and its receptor, tyrosine receptor kinase B (TrkB; also known as tropomyosin receptor kinase B). This evidence concerns the gene NTRK2 and Alzheimer disease.