The main pathological feature of Alz-heimer\'s disease (AD) is the extracellular deposition of β-amyloid (Aβ) in the brain, which forms insoluble Aβ plaques, and tau protein hyperphosphorylation in neu-rons, which forms intracellular fibrillary tangles. So far, none of the drugs targeting Aβ have been successful in the treatment of AD. Some studies have shown that brain iron deposition may be one of the important factors in AD pathogenesis; the distribution of iron deposition has been found to be consistent with the distribution of Aβ senile plaques in the brain. Effectively reducing brain iron load might therefore be a good therapeutic approach to prevent and treat AD.