Finally, the notion of an impact of Aβ on NFT formation is supported by studies in APP-transgenic mice reporting that a reduction in endogenous levels of tau can ameliorate some of the behavioral and other deficits that are mediated by Aβ [24, 25] and by the discovery that mutations in the tau gene cause autosomal dominant frontotemporal lobe dementia with a tau pathology similar to the tau pathology seen in AD but without the appearance of Aβ plaques [26]. The gene discussed is MAPT; the disease is Alzheimer disease.