Other important mechanisms contributing to the deficiency of BDNF/TrkB signalling in AD are the suppression of MAPK/ERK and PI3K/Akt pathways by sub-lethal concentrations of Aβ, without interference of TrkB-FL and PLCγ activation [85], and the disruption of BDNF-induced TrkB endocytosis. This evidence concerns the gene BDNF and Alzheimer disease.