何玉琼, 周灿灿. 金属元素与阿尔茨海默病发病机制的研究进展[J]. 环境与职业医学, 2021, 38(2): 190-194. DOI: 10.13213/j.cnki.jeom.2021.20253
引用本文: 何玉琼, 周灿灿. 金属元素与阿尔茨海默病发病机制的研究进展[J]. 环境与职业医学, 2021, 38(2): 190-194. DOI: 10.13213/j.cnki.jeom.2021.20253
HE Yuqiong, ZHOU Cancan. Advances on metal elements and mechanisms of Alzheimer's disease[J]. Journal of Environmental and Occupational Medicine, 2021, 38(2): 190-194. DOI: 10.13213/j.cnki.jeom.2021.20253
Citation: HE Yuqiong, ZHOU Cancan. Advances on metal elements and mechanisms of Alzheimer's disease[J]. Journal of Environmental and Occupational Medicine, 2021, 38(2): 190-194. DOI: 10.13213/j.cnki.jeom.2021.20253

金属元素与阿尔茨海默病发病机制的研究进展

Advances on metal elements and mechanisms of Alzheimer's disease

  • 摘要:

    阿尔茨海默病(AD)是一种进行性神经退行性疾病,也是导致老年痴呆的最主要原因之一。目前认为β-淀粉样蛋白(Aβ)的过表达和沉积以及Tau蛋白的过度磷酸化在AD发生发展中起着关键性作用,然而AD的发病机制十分复杂,至今也尚未完全阐明。近年来,越来越多的研究表明体内金属元素水平的变化与AD的发生发展密切相关。体内的金属元素可通过影响与Aβ的生成、转运和代谢相关蛋白的表达和活性,调控Aβ在脑内的生成和沉积;此外,金属元素还可通过调控Tau蛋白的过度磷酸化在AD的发生发展中发挥重要作用。本文总结了4种金属元素(铜、铝、铁、铅)在AD发生发展中的作用,阐述了其在Aβ过表达和Tau蛋白过度磷酸化中的机制,希望能为AD的预防和治疗提供一定的理论依据。

     

    Abstract:

    Alzheimer's disease (AD) is a neurodegenerative disease and also the leading cause of dementia. The over-expression and deposition of amyloid β (Aβ) and the hyperphosphorylated Tau protein play critical roles in the pathogenesis of AD. However, the underlying mechanisms of AD are complex and still not fully understood. In recent years, increasing studies have found that changes of metal element levels in the body are closely associated with the progression of AD. Metal elements could regulate the production and deposition of Aβ in the brain by affecting the expression and activities of proteins related to the production, transport, and metabolism of Aβ. In addition, metal elements also play an important role in the progression of AD by regulating the hyperphosphorylation of tau protein. In this review, we summarized the roles of four metal elements including copper, aluminum, iron, and lead in the development of AD, and illustrated their mechanisms in Aβ over-expression and Tau protein hyperphosphorylation, aiming to provide new sights and a theoretical basis for the prevention and treatment of AD.

     

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