To maximally replicate the AD-like tau pathologies, we overexpressed full-length wildtype tau (which we have well-evidenced effective in inducing AD-like tau hyperphosphorylation and accumulation34), and the more toxic truncated hTau-N368 (derived during aging or pathological conditions27) for the in vitro and in vivo studies, respectively. The gene discussed is MAPT; the disease is Alzheimer disease.