铁超载促进阿尔采末病的发展及其相关治疗

High brain iron in etiology of Alzheimer's disease and therapeutic approaches

阿尔采末病(Alzheimer's disease,AD)的早期神经病理学就表现出脑铁代谢的紊乱,并伴随有氧化应激水平的升高、β淀粉样蛋白(β-amyloid protein,Aβ)的沉积、Tau蛋白的过磷酸化以及神经元细胞周期的失控进而导致的神经元凋亡。铁代谢失控和AD之间存在很多联系,该文就铁超载促进AD发生发展的内在机制及铁螯合剂对AD的治疗进行综述,以期为AD的临床治疗提供新的策略。

Excessive iron accumulation in the brain occurs in Alzheimer＇ s disease （AD） with oxidative stress,amyloid deposition,tau phosphorylation,and neuronal cell cycle regulatory failure,leading to apoptosis.Therefore,there is a direct link between iron metabolism and AD pathogenesis. The present review elaborates on high brain iron in etiology of AD and the development of iron-chelating therapy for AD,aiming at preventing or slowing down disease evolution.