FIGURE 2.

The schematic diagram of iron participation in the deposition of Aβ plaques and tau tangles. In neurons, iron interacts with Aβ and promotes Aβ aggregation into fibrous forms. Iron can also act on the IRE site of APP mRNA, increasing the expression of endogenous APP. In addition to the interaction with Aβ, iron can also promote the phosphorylation of tau by activating the CDK5/p25 complex and GSK3β to form NFTs. At the same time, iron can also cause oxidative stress through the Fenton reaction, damaging DNA, lipids and proteins and eventually leading to cell death. The iron chelators reduce the phosphorylation of tau and inhibit the production of NFTs by inhibiting the activation of the CDK5/p25 complex and GSK3β by iron. Simultaneously, iron chelators inhibit the aggregation of Aβ monomers into toxic fibrous forms by chelating iron, delaying cell death.