Fig. 4

A proposed model illustrating the mechanism of AD progression and amelioration. The expression or alteration in activity of brain zinc transporters induce zinc dyshomeostasis, which aggravate Aß deposition, tau phosphorylation and tau-zinc binding exacerbated toxicity, increasingly promoting neuronal loss (a), while the leading compounds or drugs designed to specifically modify the expression or activity of brain zinc transport proteins have the potential to correct the disturbed zinc metabolism niche, thus leading to reduced Aß deposition, tau dissociation from microtubules and tau toxicity, which ultimately slows or prevents neuronal death in the onset and progression of AD (b)