Although most of the models do not show Tau pathology and other shedding fragments from APP processing may also influence neuron systems, transgenic rodent models with overexpression of wild type or mutated human APP can recapitulate some features of AD pathology and provide great convenience to discover more regulators involved in the onset of AD (Clarke et al., 2007; Agca et al., 2008; Leon et al., 2010; Rosen et al., 2012). The gene discussed is MAPT; the disease is Alzheimer disease.