University of Kansas Alzheimer's Disease Center, Kansas City, KS, U.S.A.
Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, KS, U.S.A.
Biochem Soc Trans. 2023 Feb 27;51(1):173-182. doi: 10.1042/BST20220518.
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.
线粒体功能障碍和 Aβ 积累是阿尔茨海默病(AD)的标志。数十年来的研究描述了线粒体功能与 Aβ 产生之间的关系。Aβ 来源于淀粉样前体蛋白(APP),而 APP 存在于线粒体中。研究表明 Aβ 可以在线粒体中产生,并被导入线粒体。APP 和 Aβ 改变线粒体功能,而线粒体功能改变 APP 产生的 Aβ。这些相互作用对 AD 病理和进展的贡献尚不清楚。在这里,我们讨论了之前的研究、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空白。