The main pathophysiological hypothesis for AD assumes that Aβ42initiates a process called the amyloid cascade.9 Although the exact mechanisms have yet to be elucidated, thetoxic effects of oligomeric forms of this peptide and its deposition as protofibrilsand fibrils in the brain to form the amyloid plaques is followed by synapticdysfunction and the appearance of intracellular neurofibrillary tangles containinghyperphosphorylated tau protein. This evidence concerns the gene MAPT and Alzheimer disease.