Abstract

Background: Existing research suggests an association between air pollution exposure and Alzheimer’s Disease (AD). However, underlying biological mechanisms are still unknown. We aimed to evaluate if air pollution exposure was associated with plasma β-amyloid (Aβ) levels. Methods: We selected 287 participants of the Three-City study who were cognitively unimpaired at 12-year follow-up. Aβ levels were measured on plasma samples stored at baseline and at 10 years (INNO-BIA plasma Aβ forms kits (Innogenetics)). Land-use regression models were used to estimate fine particulate matter (PM2.5), nitrogen dioxide (NO2) and black carbon (BC) exposure at participants’ residential address over the 5-year preceding the baseline visit. Linear regression was performed to assess the association of each pollutant with plasma Aβ levels at baseline and with their evolution over time. Results: Participants’ median age at baseline was 68.8 (IQR: 5.1), and 56.1% were women. Median levels (IQR) of plasma Aβ at baseline were 158.8 (37.5) pg/mL for Aβ1-40 and 41.4 (11.9) pg/mL for Aβ1-42. Median Aβ1-42/Aβ1-40 ratio was 0.255 (IQR: 0.065). We found that exposure to the three air pollutants was associated with decreased Aβ1-42/Aβ1-40 ratio at baseline. For instance, an IQR increase in PM2.5 (1.8 µg/m3) was associated with a 0.0119 decrease in the Aβ ratio (95% CI: -0.0209; -0.0029). There were no significant associations between air pollutants and Aβ evolution over time. Conclusion: In our cognitively unimpaired population, exposure to air pollution was associated with decreased plasma Aβ ratio at baseline. These results seem to corroborate previous ones on air pollution detrimental effect on cognition, as a decreased plasma Aβ ratio may predict AD. Further longitudinal studies using cutting edge methods to quantify plasmatic Aβ levels and brain Aβ deposits are still needed to better understand the influence of air pollution on the neuropathological process in AD. Keywords: Air pollution, Alzheimer’s Disease, Biomarkers

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