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Traffic-Related air pollution as a risk factor for dementia: no clear modifying effects of apoe ɛ4 in the betula cohort
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Section of Sustainable Health. Department of Laboratory Medicine, Lund University, Lund, Sweden. (Arcum)
Umeå University, Faculty of Social Sciences, Department of Psychology.
Umeå University, Faculty of Social Sciences, Department of Psychology.ORCID iD: 0000-0003-3606-3057
Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.ORCID iD: 0000-0002-8114-7615
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2021 (English)In: Alzheimer's disease and air pollution: the development and progression of a fatal disease from childhood and the opportunities for early prevention / [ed] Lilian Calderón-Garcidueñas, Amsterdam: IOS Press, 2021, p. 357-364Chapter in book (Refereed)
Abstract [en]

It is widely known that the apolipoprotein E (APOE) ε4 allele imposes a higher risk for Alzheimer's disease (AD). Recent evidence suggests that exposure to air pollution is also a risk factor for AD, and results from a few studies indicate that the effect of air pollution on cognitive function and dementia is stronger in APOE ε4 carriers than in non-carriers. Air pollution and interaction with APOE ε4 on AD risk thus merits further attention. We studied dementia incidence over a 15-year period from the longitudinal Betula study in Northern Sweden. As a marker for long-term exposure to traffic-related air pollution, we used modelled annual mean nitrogen oxide levels at the residential address of the participants at start of follow-up. Nitrogen oxide correlate well with fine particulate air pollution levels in the study area. We had full data on air pollution, incidence of AD and vascular dementia (VaD), APOE ε4 carrier status, and relevant confounding factors for 1,567 participants. As expected, air pollution was rather clearly associated with dementia incidence. However, there was no evidence for a modifying effect by APOE ε4 on the association (p-value for interaction > 0.30 for both total dementia (AD+VaD) and AD). The results from this study do not imply that adverse effects of air pollution on dementia incidence is limited to, or stronger in, APOE ε4 carriers than in the total population.

Place, publisher, year, edition, pages
Amsterdam: IOS Press, 2021. p. 357-364
Series
Advances in Alzheimer's Disease, ISSN 2210-5727, E-ISSN 2210-5735 ; 8
Keywords [en]
Air pollution, Alzheimer's disease, Apolipoprotein E, Dementia
National Category
Occupational Health and Environmental Health Neurology
Identifiers
URN: urn:nbn:se:umu:diva-186440DOI: 10.3233/AIAD210029Scopus ID: 2-s2.0-85110853331ISBN: 9781643681597 (electronic)ISBN: 9781643681580 (print)OAI: oai:DiVA.org:umu-186440DiVA, id: diva2:1582484
Available from: 2021-08-02 Created: 2021-08-02 Last updated: 2024-04-08Bibliographically approved

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Oudin, AnnaAndersson, JohnSundström, AnnaNordin Adolfsson, AnnelieOudin Åström, DanielAdolfsson, RolfForsberg, BertilNordin, Maria

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Oudin, AnnaAndersson, JohnSundström, AnnaNordin Adolfsson, AnnelieOudin Åström, DanielAdolfsson, RolfForsberg, BertilNordin, Maria
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Section of Sustainable HealthDepartment of PsychologyPsychiatry
Occupational Health and Environmental HealthNeurology

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