Long-Term Exposure to PM10 and in vivo Alzheimer’s Disease Pathologies

Jun Ho Lee, M. Byun, D. Yi, K. Ko, S. Jeon, B. Sohn, Jun-Young Lee, Younghwan Lee, Haejung Joung, D. Y. Lee
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引用次数: 1

Abstract

Background: Previous studies indicated an association between Alzheimer’s disease (AD) dementia and air particulate matter (PM) with aerodynamic diameter <10 μm (PM10), as well as smaller PM. Limited information, however, is available for the neuropathological links underlying such association. Objective: This study aimed to investigate the relationship between long-term PM10 exposure and in vivo pathologies of AD using multimodal neuroimaging. Methods: The study population consisted of 309 older adults without dementia (191 cognitively normal and 118 mild cognitive impairment individuals), who lived in Republic of Korea. Participants underwent comprehensive clinical assessments, 11C-Pittsburg compound B (PiB) positron emission tomography (PET), and magnetic resonance imaging scans. A subset of 78 participants also underwent 18F-AV-1451 tau PET evaluation. The mean concentration of PM with aerodynamic diameter <10 μm over the past 5 years (PM10mean) collected from air pollution surveillance stations were matched to each participant’s residence. Results: In this non-demented study population, of which 62% were cognitively normal and 38% were in mild cognitive impairment state, exposure to the highest tertile of PM10mean was associated with increased risk of amyloid-β (Aβ) positivity (odds ratio 2.19, 95% confidence interval 1.13 to 4.26) even after controlling all potential confounders. In contrast, there was no significant associations between PM10mean exposure and tau accumulation. AD signature cortical thickness and white matter hyperintensity volume were also not associated with PM10mean exposure. Conclusion: The findings suggest that long-term exposure to PM10 may contribute to pathological Aβ deposition.
长期暴露于PM10与体内阿尔茨海默病病理
背景:已有研究表明,阿尔茨海默病(AD)痴呆与空气动力学直径<10 μm (PM10)的空气颗粒物(PM)以及较小的PM之间存在关联。然而,对于这种关联背后的神经病理联系,信息有限。目的:本研究旨在通过多模态神经影像学研究长期PM10暴露与AD体内病理的关系。方法:研究人群包括居住在大韩民国的309名无痴呆的老年人(191名认知正常,118名轻度认知障碍)。参与者接受了全面的临床评估,11c -匹兹堡化合物B (PiB)正电子发射断层扫描(PET)和磁共振成像扫描。78名参与者也接受了18F-AV-1451 tau PET评估。空气污染监测站近5年空气动力学直径<10 μm的PM平均浓度(PM10mean)与每个参与者的居住地相匹配。结果:在这个非痴呆的研究人群中,62%的人认知正常,38%的人处于轻度认知障碍状态,即使在控制了所有潜在的混杂因素后,暴露于pm10均值最高的五位数也与淀粉样蛋白-β (Aβ)阳性的风险增加相关(优势比2.19,95%置信区间1.13至4.26)。相比之下,pm10平均暴露与tau积累之间没有显着关联。AD特征皮层厚度和白质高强度体积也与pm10平均暴露无关。结论:长期暴露于PM10可能导致Aβ的病理沉积。
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