Interactions between amyloid, amyloid precursor protein, and mitochondria.
Interactions between amyloid, amyloid precursor protein, and mitochondria.
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DOI：
10.1042/bst20220518
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发表时间：
2023-02-27
影响因子：
3.9
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中科院分区：
文献类型：
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线粒体功能障碍和Aβ积聚是阿尔茨海默病（AD）的标志。几十年的研究描述了线粒体功能和Aβ产生之间的关系。淀粉样前体蛋白（APP），其中产生Aβ，被发现在线粒体内。研究表明，Aβ可以在线粒体中产生并输入线粒体。APP和Aβ改变线粒体功能，而线粒体功能改变APP产生的Aβ。这些相互作用在AD病理和进展中的作用尚不清楚。在这里，我们讨论了先前的研究，这些研究的严谨性，以及APP，Aβ和线粒体之间关系的关键知识差距。
Mitochondrial dysfunction and Aβ accumulation are hallmarks of Alzheimer's disease (AD). Decades of research describe a relationship between mitochondrial function and Aβ production. Amyloid precursor protein (APP), of which Aβ is generated from, is found within mitochondria. Studies suggest Aβ can be generated in mitochondria and imported into mitochondria. APP and Aβ alter mitochondrial function, while mitochondrial function alters Aβ production from APP. The role these interactions contribute to AD pathology and progression are unknown. Here, we discuss prior research, the rigor of those studies, and the critical knowledge gaps of relationships between APP, Aβ, and mitochondria.