Indian Scientific Education and Technology Foundation, Lucknow, 226002, India.
Saint James School of Medicine, Park Ridge, IL 60068, USA.
Metallomics. 2022 Jun 13;14(6). doi: 10.1093/mtomcs/mfac018.
The link between bio-metals, Alzheimer's disease (AD), and its associated protein, amyloid-β (Aβ), is very complex and one of the most studied aspects currently. Alzheimer's disease, a progressive neurodegenerative disease, is proposed to occurs due to the misfolding and aggregation of Aβ. Dyshomeostasis of metal ions and their interaction with Aβ has largely been implicated in AD. Copper plays a crucial role in amyloid-β toxicity, and AD development potentially occurs through direct interaction with the copper-binding motif of APP and different amino acid residues of Aβ. Previous reports suggest that high levels of copper accumulation in the AD brain result in modulation of toxic Aβ peptide levels, implicating the role of copper in the pathophysiology of AD. In this review, we explore the possible mode of copper ion interaction with Aβ, which accelerates the kinetics of fibril formation and promote amyloid-β mediated cell toxicity in Alzheimer's disease and the potential use of various copper chelators in the prevention of copper-mediated Aβ toxicity.
Short Twitter Statement: Authors explore copper ion interaction w/ Aβ and kinetics of fibril formation in promoting amyloid-β mediated cell toxicity in Alzheimer's disease and the potential use of copper chelators in the prevention of copper-mediated Aβ toxicity.
Authors explore copper ion interaction w/Aβ and kinetics of fibril formation in promoting amyloid-β mediated cell toxicity in Alzheimer's disease and the potential use of copper chelators in the prevention of copper-mediated Aβ toxicity.
生物金属、阿尔茨海默病（AD）及其相关蛋白淀粉样β（Aβ）之间的联系非常复杂，是目前研究最多的方面之一。阿尔茨海默病是一种进行性神经退行性疾病，据推测是由于 Aβ 的错误折叠和聚集而发生的。金属离子的动态平衡及其与 Aβ 的相互作用在很大程度上与 AD 有关。铜在淀粉样β毒性中起着至关重要的作用，AD 的发展可能是通过 APP 的铜结合基序与 Aβ 的不同氨基酸残基的直接相互作用发生的。先前的报告表明，AD 大脑中铜的大量积累导致毒性 Aβ 肽水平的调节，这表明铜在 AD 的病理生理学中起作用。在这篇综述中，我们探讨了铜离子与 Aβ 相互作用的可能模式，这种相互作用加速了纤维形成的动力学，并促进了阿尔茨海默病中淀粉样β介导的细胞毒性，以及各种铜螯合剂在预防铜介导的 Aβ 毒性中的潜在用途。
短推文陈述：作者探索铜离子与 Aβ 的相互作用以及原纤维形成的动力学在促进阿尔茨海默病中淀粉样β介导的细胞毒性中的作用，以及铜螯合剂在预防铜介导的 Aβ 毒性中的潜在用途。
作者探索铜离子与 Aβ 的相互作用以及原纤维形成的动力学在促进阿尔茨海默病中淀粉样β介导的细胞毒性中的作用，以及铜螯合剂在预防铜介导的 Aβ 毒性中的潜在用途。
