Remarkably, this fragment resulting from Aβ1–40 and Aβ1–42 proteolysis appears extremely toxic, with an important lifespan in brain tissues and could significantly contribute to the overall toxicity and therefore to the maintenance of the progressive neurodegeneration processes observed in AD, through particularly an inhibition of BDNF, an increase of apoptotic processes, a glucocorticoid hypersecretion, and the induction of the amyloid pathway and abnormal phosphorylation of Tau. This evidence concerns the gene BDNF and Alzheimer disease.