ISSN 0371-0874, CN 31-1352/Q

过刊浏览

环境污染物与阿尔茨海默病

郭宝1, 巴乾1,2,*

1上海交通大学公共卫生学院,上海 200025;2上海中医药大学附属市中医医院实验中心,上海 200071

摘要

阿尔茨海默病(Alzheimer’s disease, AD)是一种神经退行性疾病,其特征是进行性认知障碍,关于AD的致病机制假说主要有β-淀粉样蛋白假说、Tau蛋白异常磷酸化假说和神经炎症假说等。近几年,环境污染物被认为是促进神经系统功能障碍的重要因素。常见的环境污染物包括重金属、农药、多氯联苯、微塑料和空气污染物等,这些都被证明具有神经毒性。本综述不仅讨论了将环境污染与AD联系起来的流行病学和动物实验研究,还总结了相关毒物的作用机制,为研究环境污染物与AD之间的相互联系提供了有益视角。

关键词: 阿尔茨海默病; 环境污染物; β-淀粉样蛋白; Tau蛋白异常磷酸化; 神经炎症

Environmental pollutants and Alzheimer’s disease

GUO Bao1, BA Qian1,2,*

1Shanghai Jiao Tong University School of Public Health, Shanghai 200025, China;2Laboratory Center, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200071, China

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive cognitive impairment. The main hypotheses about the pathogenesis of AD include the hypothesis of β-amyloid protein, the hypothesis of abnormal phosphorylation of Tau protein, and the hypothesis of neuroinflammation. In recent years, environmental pollutants have been considered as an important factor in causing neurological dysfunction. Common environmental pollutants include heavy metals, pesticides, polychlorinated biphenyls, microplastics, and air pollutants, all of which have been proven to have neurotoxicity. In this review, we not only discussed epidemiological and animal experimental studies that link environmental pollution with AD, but also summarized the mechanisms of action of relevant toxins, providing insights for studying the interrelationships between environmental pollutants and AD.

Key words: Alzheimer’s disease; environmental pollutants; β-amyloid protein; Tau protein abnormal phosphorylation; neuroinflammation

收稿日期:  录用日期:

通讯作者:巴乾  E-mail: qba@shsmu.edu.cn

DOI: 10.13294/j.aps.2023.0080

引用本文:

郭宝, 巴乾. 环境污染物与阿尔茨海默病[J]. 生理学报 2023; 75 (6): 740-766.

GUO Bao, BA Qian. Environmental pollutants and Alzheimer’s disease. Acta Physiol Sin 2023; 75 (6): 740-766 (in Chinese with English abstract).