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Aβ-ganglioside interactions in the pathogenesis of Alzheimer's disease.
Biochimica et Biophysica Acta (BBA) - Biomembranes ( IF 2.8 ) Pub Date : 2020-03-03 , DOI: 10.1016/j.bbamem.2020.183233
Katsumi Matsuzaki 1
Affiliation  

It is widely accepted that the abnormal self-association of amyloid β-protein (Aβ) is central to the pathogenesis of Alzheimer's disease, the most common form of dementia. Accumulating evidence, both in vivo and in vitro, suggests that the binding of Aβ to gangliosides, especially monosialoganglioside GM1, plays an important role in the aggregation of Aβ. This review summarizes the molecular details of the binding of Aβ to ganglioside-containing membranes and subsequent structural changes, as revealed by liposomal and cellular studies. Furthermore, mechanisms of cytotoxicity by aggregated Aβ are also discussed.

中文翻译:

阿尔茨海默氏病发病机理中的Aβ神经节苷脂相互作用。

普遍认为,淀粉样β蛋白(Aβ)的异常自缔合是阿尔茨海默氏病(痴呆的最常见形式)的发病机制的核心。体内和体外的越来越多的证据表明,Aβ与神经节苷脂,特别是单唾液酸神经节苷脂GM1的结合在Aβ的聚集中起重要作用。这项综述总结了脂质体和细胞研究揭示的Aβ与含有神经节苷脂的膜结合的分子细节以及随后的结构变化。此外,还讨论了聚集的Aβ引起的细胞毒性机制。
更新日期:2020-03-03
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