In AD pathogenesis, there is progressive dysregulation of neurotrophin synthesis, release and function [29], including aberrant BDNF/tropomyosin receptor kinase (Trk)B and neurotrophin-3 (NT-3)/TrkC signaling [30], which highlight their importance as potential treatments/targets for alleviating AD-related neuropathology. This evidence concerns the gene BDNF and Alzheimer disease.