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观点:神经原纤维缠结与淀粉样斑块形成之间的串扰。

Viewpoint: Crosstalks between neurofibrillary tangles and amyloid plaque formation.

机构信息

Department of Cell Biology and Anatomy, Southern Alberta Cancer Research and Hotchkiss Brain Institutes, University of Calgary, Alberta, Canada.

出版信息

Ageing Res Rev. 2013 Jan;12(1):174-81. doi: 10.1016/j.arr.2012.06.002. Epub 2012 Jun 19.

Abstract

Since its discovery, the hallmarks of Alzheimer's disease (AD) brain have been recognised as the formation of amyloid plaques and neurofibrillary tangles (NFTs). Mounting evidence has suggested the active interplay between the two pathways. Studies have shown that β-amyloid (Aβ) can be internalized and generated intracellularly, accelerating NFT formation. Conversely, tau elements in NFTs are observed to affect Aβ and amyloid plaque formation. Yet the precise mechanisms which link the pathologies of the two brain lesions remain elusive. In this review, we discuss recent evidence that support five putative mechanisms by which crosstalk occurs between amyloid plaque and NFT formation in AD pathogenesis. Understanding the crosstalks in the formation of AD pathologies could provide new clues for the development of novel therapeutic strategies to delay or halt the progression of AD.

摘要

自发现以来,阿尔茨海默病(AD)大脑的标志性特征已被认为是淀粉样斑块和神经原纤维缠结(NFTs)的形成。越来越多的证据表明这两种途径之间存在着积极的相互作用。研究表明,β-淀粉样蛋白(Aβ)可以被内化并在细胞内产生,从而加速 NFT 的形成。相反,NFT 中的 tau 元素被观察到影响 Aβ和淀粉样斑块的形成。然而,将两种脑损伤的病理联系起来的确切机制仍然难以捉摸。在这篇综述中,我们讨论了最近的证据,这些证据支持了 AD 发病机制中淀粉样斑块和 NFT 形成之间发生五种可能的相互作用机制。了解 AD 病理形成中的相互作用可能为开发新的治疗策略提供新的线索,以延缓或阻止 AD 的进展。

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