To avoid the potential disturbing of tau phosphorylation and degradation by APP and PSEN1 genes mutations, and the impact of human tau expression on murine embryonic development in 3 × Tg AD mice,25,26 we tested the efficiency of DEPTAC in a self-developed transgenic mouse line named Tau368 mice, in which the neurotoxic27 human tau N-terminal 1–368 fragment (hTau-N368) is overexpressed under the control of neuron-specific enolase (NSE) promoter together with a tet-on system (Fig. 3a). Here, ENO2 is linked to Alzheimer disease.