To accomplish this task, we used a triple transgenic mouse model of AD (3xTg-AD), a strain homozygous for the Psen1 mutation and homozygous for the co-injected APPSwe and tauP301L transgenes, which presents an age-dependent increase of Aβ oligomer accumulation, extracellular plaques in the cortex and the hippocampus, and tau pathology paralleled by learning and memory impairment [25]. This evidence concerns the gene MAPT and Alzheimer disease.