Recently study has found a new form of copper-dependent death called cuproptosis, which differs from apoptosis, ferroptosis, and necrosis. The main process of cuproptosis is copper directly combined with lipid-acetylated proteins in the TCA cycle of mitochondrial response, leading to the aggregation of lipid-acetylated proteins and the loss of Fe-S cluster proteins, resulting in mitochondrial dysfunction, and eventually causing cell death. Previous studies demonstrated that an imbalance in copper homeostasis exacerbates the pathological progression of Alzheimer's disease (AD) through the induction of oxidative stress, inflammatory response, and the accumulation of Aβ deposition and tau protein hyperphosphorylation. However, the underlying mechanisms remains to be elucidated. More importantly, research identifies the role of cuproptosis and further elucidates the underlying molecular mechanisms in AD. This review summarized the effects of copper metabolism on AD pathology, the characteristics and mechanism of cuproptosis and we discuss the significance of cuproptosis in the pathogenesis of AD.
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