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错误折叠的 Aβ 寡聚物的难以捉摸的性质和诊断。

The elusive nature and diagnostics of misfolded Aβ oligomers.

机构信息

Biotechnology Department, National Physical Laboratory Teddington, UK.

Basic Medical Sciences, St. George's University of London London, UK.

出版信息

Front Chem. 2015 Mar 19;3:17. doi: 10.3389/fchem.2015.00017. eCollection 2015.

Abstract

Amyloid-beta (Aβ) peptide oligomers are believed to be the causative agents of Alzheimer's disease (AD). Though post-mortem examination shows that insoluble fibrils are deposited in the brains of AD patients in the form of intracellular (tangles) and extracellular (plaques) deposits, it has been observed that cognitive impairment is linked to synaptic dysfunction in the stages of the illness well before the appearance of these mature deposits. Increasing evidence suggests that the most toxic forms of Aβ are soluble low-oligomer ligands whose amounts better correlate with the extent of cognitive loss in patients than the amounts of fibrillar insoluble forms. Therefore, these ligands hold the key to a better understanding of AD prompting the search for clearer correlations between their structure and toxicity. The importance of such correlations and their diagnostic value for the early diagnosis of AD is discussed here with a particular emphasis on the transient nature and structural plasticity of misfolded Aβ oligomers.

摘要

淀粉样蛋白-β(Aβ)肽寡聚体被认为是阿尔茨海默病(AD)的致病因子。虽然尸检显示,不溶性原纤维以细胞内(缠结)和细胞外(斑块)沉积物的形式沉积在 AD 患者的大脑中,但已经观察到认知障碍与这些成熟沉积物出现之前疾病阶段的突触功能障碍有关。越来越多的证据表明,Aβ的最毒形式是可溶性低寡聚配体,其数量与患者认知丧失的程度比纤维状不溶性形式的数量更好地相关。因此,这些配体是更好地理解 AD 的关键,促使人们寻找它们的结构与毒性之间更清晰的相关性。本文讨论了这种相关性的重要性及其对 AD 的早期诊断的诊断价值,特别强调了错误折叠的 Aβ寡聚体的瞬时性质和结构可塑性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36a0/4365737/4fe98f2cdc7c/fchem-03-00017-g0001.jpg

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