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Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by the formation of senile plaques and neurofibrillary fiber tangles. Studies have shown that increased regional iron loading in the brain, dysregulation of iron homeostasis in the body, oxidative stress, and protein and lipid oxidation are all involved in the pathogenesis of AD. Ferroptosis, an iron-dependent, lipid peroxidation-driven form of regulated cell death, is increasingly implicated in the pathological process of AD, and some new compounds targeting ferroptosis demonstrate therapeutic efficacy in both cellular and animal models of AD. Therefore, this article systematically summarizes recent advances in the role of ferroptosis in AD pathogenesis and highlights progress in targeting ferroptosis for AD treatment, providing insights for future therapeutic and preventive strategies.
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