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A proposed model illustrating the mechanism that underlies NTZ in the amelioration of AD pathology. NTZ stimulated autophagy and promoted Aβ clearance by inhibiting both PI3K/AKT/mTOR/ULK1 and NQO1/mTOR/ULK1 signaling pathways. NTZ was capable of repressing tau hyperphosphorylation involving inhibition of PI3K/AKT/GSK3β pathway and attenuating LPS-induced inflammation by inhibiting PI3K/AKT/IκB/NFκB signaling
