Air pollution and biomarkers of Alzheimer's disease in cognitively unimpaired individuals: Epidemiology: Effects of air pollution on cognition. (7th December 2020)

• Record Type: Journal Article
• Authors: Crous‐Bou, Marta; Alemany, Silvia; Vilor‐Tejedor, Natalia; Milà‐Alomà, Marta; Suárez‐Calvet, Marc; Salvadó, Gemma; Cirach, Marta; Arenaza‐Urquijo, Eider M; Sánchez‐Benavides, Gonzalo; Grau‐Rivera, Oriol; Minguillón, Carolina; Fauria, Karine; Gispert, Juan Domingo; Nieuwenhuijsen, Mark; Zetterberg, Henrik; Blennow, Kaj; Kollmorgen, Gwendlyn; Eichenlaub, Udo; Sunyer, Jordi; Molinuevo, Jose Luis
• Is Part Of: Alzheimer's & dementia. Volume 16(2020)Supplement 10
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-12-07
• Subjects: Alzheimer's disease -- Periodicals; Alzheimer Disease -- Periodicals; Dementia -- Periodicals; Démence; Maladie d'Alzheimer; Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 616.83
• DOI: 10.1002/alz.044802
• Languages: English
• ISSNs: 1552-5260

Abstract

Abstract: Background: Air quality might contribute to incidence of dementia‐related disorders, including Alzheimer's disease (AD). The aim of our study was to examine whether air pollution may be associated with abnormal concentrations of AD cerebrospinal fluid (CSF) and neuroimaging biomarkers in cognitively unimpaired individuals at increased risk of AD. Additionally, potential effect modification by amyloid‐β(Aβ) and APOE ‐ɛ4 status was investigated. Methods: The ALFA (ALzheimer and FAmilies) study is a prospective cohort of cognitively unimpaired, middle‐aged subjects, many AD patients' offspring. Land Use Regression models were used to estimate residential exposure to air pollutants including nitrogen oxides (NO2, NOx ) and particulate matter (PM2.5, PM2.5 abs, PM10, PM coarse). For a subset, we measured CSF levels of Aβ42, Aβ40, p‐tau, t‐tau and neurofilament light (NfL) using NeuroToolKit and Elecsys ® immunoassays (Roche Diagnostics). They also underwent a [ 18 F]flutemetamol amyloid PET scan to assess cerebral amyloid load (Centiloid). A total of 148 participants (all residents of Barcelona) with data available on exposure to air pollutants and core AD biomarkers were included in this cross‐sectional analysis. Multiple linear regression models were used to test the association between exposure to air pollutants and biomarkers. Age, sex, years of education and APOE ‐ɛ4 status were included as potential confounders. To test for effect modification, Aβ positivity was defined by an Aβ42/Aβ40 ratio<0.071. Stratified analyses by APOE genotype were also performed. Results: Greater exposure to air pollutants was associated with increased levels of CSF p‐tau, t‐tau and NfL, and reduced Aβ42/40 ratio. Additionally, higher exposure to nitrogen oxides was significantly associated with increased Aβ deposition in the brain (Figure1;*p<0.05). Such associations were driven by Aβ‐negative individuals (p‐interaction<0.05) (Figure 2;*p<0.05). Furthermore, the association between increased exposure to air pollutants and Ab deposition was only seen in APOE ‐ɛ4 non‐carriers, while the positive association between exposure to air pollutants and CSF p‐tau, t‐tau and NfL was only observed among APOE ‐ɛ4 carriers (Figure 3;*p<0.05). Conclusion: In a population of cognitively unimpaired adults with increased risk of AD, exposure to air pollution is associated with abnormal core AD biomarker results. Further research is granted to elucidate the mechanisms involved in such associations.