Ma Ya-Hui, Chen Hua-Shuai, Liu Cong, Feng Qiu-Shi, Feng Lei, Zhang Ya-Ru, Hu Hao, Dong Qiang, Tan Lan, Kan Hai-Dong, Zhang Can, Suckling John, Zeng Yi, Chen Ren-Jie, Yu Jin-Tai
Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China; Department of Neurology and Institute of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.
School of Business, Xiangtan University, Xiangtan, Hunan, China.
Biol Psychiatry. 2023 May 1;93(9):780-789. doi: 10.1016/j.biopsych.2022.05.017. Epub 2022 May 18.
Air pollution induces neurotoxic reactions and may exert adverse effects on cognitive health. We aimed to investigate whether air pollutants accelerate cognitive decline and affect neurobiological signatures of Alzheimer's disease (AD).
We used a population-based cohort from the Chinese Longitudinal Healthy Longevity Survey with 31,573 participants and a 10-year follow-up (5878 cognitively unimpaired individuals in Chinese Longitudinal Healthy Longevity Survey followed for 5.95 ± 2.87 years), and biomarker-based data from the Chinese Alzheimer's Biomarker and Lifestyle study including 1131 participants who underwent cerebrospinal fluid measurements of AD-related amyloid-β (Aβ) and tau proteins. Cognitive impairment was determined by education-corrected performance on the China-Modified Mini-Mental State Examination. Annual exposures to fine particulate matter (PM), ground-level ozone (O), and nitrogen dioxide (NO) were estimated at areas of residence. Exposures were aggregated as 2-year averages preceding enrollments using Cox proportional hazards or linear models.
Long-term exposure to PM (per 20 μg/m) increased the risk of cognitive impairment (hazard ratio, 1.100; 95% CI: 1.026-1.180), and similar associations were observed from separate cross-sectional analyses. Exposures to O and NO yielded elevated risk but with nonsignificant estimates. Individuals exposed to high PM manifested increased amyloid burdens as reflected by cerebrospinal fluid-AD biomarkers. Moreover, PM exposure-associated decline in global cognition was partly explained by amyloid pathology as measured by cerebrospinal fluid-Aβ/Aβ, P-tau/Aβ, and T-tau/Aβ, with mediation proportions ranging from 16.95% to 21.64%.
Long-term exposure to PM contributed to the development of cognitive decline, which may be partly explained by brain amyloid accumulation indicative of increased AD risk.
空气污染会引发神经毒性反应，并可能对认知健康产生不利影响。我们旨在研究空气污染物是否会加速认知衰退，并影响阿尔茨海默病（AD）的神经生物学特征。
我们使用了来自中国老年健康影响因素跟踪调查的基于人群的队列，该队列有31573名参与者，并进行了为期10年的随访（中国老年健康影响因素跟踪调查中的5878名认知未受损个体随访了5.95±2.87年），以及来自中国阿尔茨海默病生物标志物与生活方式研究的基于生物标志物的数据，该研究包括1131名接受了与AD相关的淀粉样蛋白β（Aβ）和tau蛋白脑脊液测量的参与者。认知障碍通过中国修订版简易精神状态检查表中经教育校正的表现来确定。根据居住地区估计每年细颗粒物（PM）、地面臭氧（O）和二氧化氮（NO）的暴露量。使用Cox比例风险模型或线性模型将暴露量汇总为入组前的2年平均值。
长期暴露于PM（每20μg/m）会增加认知障碍的风险（风险比，1.100；95%置信区间：1.026 - 1.180），并且在单独的横断面分析中也观察到了类似的关联。暴露于O和NO会增加风险，但估计值不显著。暴露于高浓度PM的个体脑脊液AD生物标志物反映出淀粉样蛋白负担增加。此外，脑脊液Aβ/Aβ、P-tau/Aβ和T-tau/Aβ测量的淀粉样蛋白病理部分解释了与PM暴露相关的整体认知下降，中介比例范围为16.95%至21.64%。
长期暴露于PM会导致认知衰退的发展，这可能部分由指示AD风险增加的脑淀粉样蛋白积累来解释。
