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![Unraveling the tau puzzle: a review of mechanistic targets and therapeutic interventions to prevent tau pathology in Alzheimer's disease](https://image.oaes.cc/48be6d03-d7e6-492c-8b63-9c49991c8e0a/and3020.fig.3.jpg)
Figure 3. Therapeutic pathways to mediate post-translational tau modifications. (A) GABAAR inhibitors bind to GABAAR to inhibit the hyperphosphorylation of tau[22,35]. GSK-3β inhibitors likewise block tau hyperphosphorylation[36-40]; (B) Acetylated tau exhibits lower levels of proteasomal degradation. SIRT1 promoters inhibit the acetylation of tau to enable pathologic tau degradation in the proteasome[69-71]; (C) Upregulation of 5-HT4 promotes the ubiquitination of tau to promote proteasomal breakdown on pathologic tau[69,72-74]; (D) Upregulation of O-GlcNAcase promotes the O-GlcNAcylation of tau to lower levels of tau hyperphosphorylation[34,75-77]; (E) The drugs LMTM and ACI-3024 inhibit tau aggregation[34,78-80]. Created with BioRender.com. GABAAR: γ-aminobutyric acid sub-type A receptor; GSK-3β: glycogen synthase kinase-3β; LMTM: leuco-methylthioninium bis(hydromethanesulphonate); SIRT1: Deacetylase protein sirtuin 1.