Council for Nutritional and Environmental Medicine, Toften 24, 8610, Mo i Rana, Norway.
Faculty of Health and Social Science, Inland Norway University of Applied Sciences, Elverum, Norway.
Mol Neurobiol. 2019 Oct;56(10):7032-7044. doi: 10.1007/s12035-019-1563-9. Epub 2019 Apr 9.
Alzheimer's disease (AD) is known as a devastating neurodegenerative disorder in aged subjects, which is related to multiple heterogeneous genetic factors. The two basic pathological aspects of AD are related to amyloid beta (Aβ) peptides and tau proteins. Some researchers have demonstrated plaques and tangles as apparently primary lesions. Also, experimental data propose that these two lesions are intimately related. In the present review, we highlight some molecular mechanisms linking tau and Aβ toxicities involving oxidative stress, aging, Aβ turnover, the contribution of thiol groups, and the role mitochondrial activities in the AD pathogenesis. Understanding the interplay of these mechanisms as parts of common pathophysiological pathways could reveal molecular targets to control or even treat AD.
阿尔茨海默病（AD）是一种发生于老年人群的破坏性神经退行性疾病，与多种异质遗传因素有关。AD 的两个基本病理方面与淀粉样β（Aβ）肽和tau 蛋白有关。一些研究人员已经证明斑块和缠结是明显的原发性病变。此外，实验数据表明这两种病变密切相关。在本综述中，我们强调了一些将 tau 和 Aβ毒性联系起来的分子机制，涉及氧化应激、衰老、Aβ 周转、巯基的贡献以及线粒体活性在 AD 发病机制中的作用。了解这些机制的相互作用作为共同病理生理途径的一部分，可以揭示控制甚至治疗 AD 的分子靶点。
