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Amyloid A beta(42), a promoter of magnetite nanoparticle formation in Alzheimer's disease

机译:淀粉样蛋白A beta(42),阿尔茨海默氏病中磁铁矿纳米颗粒形成的促进剂

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摘要

The accumulation of iron oxides-mainly magnetite-with amyloid peptide is a key process in the development of Alzheimer's disease (AD). However, the mechanism for biogeneration of magnetite inside the brain of someone with AD is still unclear. The iron-storing protein ferritin has been identified as the main magnetite-storing molecule. However, accumulations of magnetite in AD are not correlated with an increase in ferritin, leaving this question unresolved. Here we demonstrate the key role of amyloid peptide A beta(42), one of the main hallmarks of AD, in the generation of magnetite nanoparticles in the absence of ferritin. The capacity of amyloid peptide to bind and concentrate iron hydroxides, the basis for the formation of magnetite, benefits the spontaneous synthesis of these nanoparticles, even under unfavorable conditions for their formation. Using scanning and transmission electron microscopy, electron energy loss spectroscopy and magnetic force microscopy we characterized the capacity of amyloid peptide A beta(42) to promote magnetite formation.
机译:氧化铁(主要是磁铁矿)和淀粉样肽的积累是阿尔茨海默氏病(AD)发展的关键过程。但是,AD患者大脑内磁铁矿生物生成的机制仍不清楚。储铁蛋白铁蛋白已被确定为主要的储磁铁分子。但是,AD中磁铁矿的积累与铁蛋白的增加无关,因此这个问题尚未解决。在这里,我们证明了淀粉样蛋白肽A beta(42)(AD的主要标志之一)在缺少铁蛋白的情况下在磁铁矿纳米颗粒生成中的关键作用。淀粉状肽结合和浓缩氢氧化铁(形成磁铁矿的基础)的能力有利于这些纳米颗粒的自发合成,即使在不利的条件下也是如此。使用扫描和透射电子显微镜,电子能量损失谱和磁力显微镜,我们表征了淀粉样肽A beta(42)促进磁铁矿形成的能力。

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