In a most simplified way, we can say that much of the symptomatology that characterizes Alzheimer's disease (AD) can be attributed to a cascade of toxic events initiated by the presence in the interstitial space of the brain of oligomers of the β‐amyloid peptide (Aβ) peptide, a cleavage by‐product of the Amyloid precursor protein (APP). This evidence concerns the gene APP and Alzheimer disease.