Figure 12.

A proposed model showing the amelioration of THA on Aβ/Tau pathology. Senile plaques formed by Aβ deposition and NFTs composed of hyperphosphorylated Tau are believed to be two major hallmarks of AD pathology. THΑ stimulated either PI₃K/AKT/mTOR- or AMPK/raptor/mTOR signaling-mediated autophagy in promoting Aβ clearance as both a PI₃K inhibitor and an AMPK indirect activator. THA restricted Aβ production as a suppressor against PERK/eIF2α-mediated BACE1 expression. Additionally, THA functioned as a GSK3β inhibitor, repressing Tau hyperphosphorylation.