线粒体
细胞外
细胞内
淀粉样蛋白(真菌学)
肽
阿尔茨海默病
细胞生物学
生物
淀粉样前体蛋白
P3肽
自噬
生物化学
疾病
化学
医学
病理
细胞凋亡
植物
作者
Ondřej Benek,Laura Aitken,Lukáš Hroch,Kamil Kuča,Frank J. Gunn‐Moore,Kamil Musílek
标识
DOI:10.2174/0929867322666150114163051
摘要
The amyloid-β peptide (Aβ) has been associated with Alzheimer's disease (AD) for decades. The original amyloid cascade hypothesis declared that the insoluble extracellular plaques were responsible for Aβ toxicity. Later, this hypothesis has been updated and soluble intracellular Aβ forms and their effects within the cell have come into focus.Mitochondrial dysfunction plays an important role in the pathophysiology of AD. Aβ was detected inside mitochondria and several mitochondrial proteins were found to interact directly with Aβ. Such interactionscan affecta protein's function and cause damage to the mitochondria and finally to the whole cell.This review summarizes the current knowledge of mitochondrial proteins directly interacting with Aβ and discusses their significance for the development of therapeutics in the treatment of AD.
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