Consistent with this hypothesis, both intracerebral infusion of Aβ in FTDP-17 tau mutation P301L-expressing tg mice and crossing these animals with APP tg 257G mutations, showed exacerbation of neurofibrillary pathology [18, 19], and in the 3 × tg-AD mice, Aβ deposition was found to precede neurofibrillary pathology, being more severe than in double tg 2× tg-AD mice [20, 21]. This evidence concerns the gene MAPT and Alzheimer disease.