The protein abundance of phosphorylated-tau T-231, β-amyloid and amyloid precursor protein was increased in STZ-treated cells (Fig. S1c–f) and p-tau at T231 protein level was increased significantly in Aβ1–42 treated N2A cells, confirming the induction of AD pathogenesis in neuronal cells (Fig. 1c, e). The gene discussed is MAPT; the disease is Alzheimer disease.