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      A national cohort study (2000–2018) of long-term air pollution exposure and incident dementia in older adults in the United States

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          Abstract

          Air pollution may increase risk of Alzheimer’s disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000–2018), combined with high-resolution air pollution datasets, to investigate the association of long-term exposure to ambient fine particulate matter (PM 2.5), nitrogen dioxide (NO 2), and ozone (O 3) with dementia and AD incidence, respectively. We identified ~2.0 million incident dementia cases ( N = 12,233,371; dementia cohort) and ~0.8 million incident AD cases ( N = 12,456,447; AD cohort). Per interquartile range (IQR) increase in the 5-year average PM 2.5 (3.2 µg/m 3), NO 2 (11.6 ppb), and warm-season O 3 (5.3 ppb) over the past 5 years prior to diagnosis, the hazard ratios (HRs) were 1.060 (95% confidence interval [CI]: 1.054, 1.066), 1.019 (95% CI: 1.012, 1.026), and 0.990 (95% CI: 0.987, 0.993) for incident dementias, and 1.078 (95% CI: 1.070, 1.086), 1.031 (95% CI: 1.023, 1.039), and 0.982 (95%CI: 0.977, 0.986) for incident AD, respectively, for the three pollutants. For both outcomes, concentration-response relationships for PM 2.5 and NO 2 were approximately linear. Our study suggests that exposures to PM 2.5 and NO 2 are associated with incidence of dementia and AD.

          Abstract

          Air pollution has been linked to neurodegenerative disease. Here the authors carried out a population-based cohort study to investigate the association between long-term exposure to PM 2.5, NO 2, and warm-season O 3 on dementia and Alzheimer’s disease incidence in the United States.

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          Most cited references47

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          Dementia prevention, intervention, and care

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            The Lancet Commission on pollution and health

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              Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade.

              Currently available evidence strongly supports the position that the initiating event in Alzheimer's disease (AD) is related to abnormal processing of beta-amyloid (Abeta) peptide, ultimately leading to formation of Abeta plaques in the brain. This process occurs while individuals are still cognitively normal. Biomarkers of brain beta-amyloidosis are reductions in CSF Abeta(42) and increased amyloid PET tracer retention. After a lag period, which varies from patient to patient, neuronal dysfunction and neurodegeneration become the dominant pathological processes. Biomarkers of neuronal injury and neurodegeneration are increased CSF tau and structural MRI measures of cerebral atrophy. Neurodegeneration is accompanied by synaptic dysfunction, which is indicated by decreased fluorodeoxyglucose uptake on PET. We propose a model that relates disease stage to AD biomarkers in which Abeta biomarkers become abnormal first, before neurodegenerative biomarkers and cognitive symptoms, and neurodegenerative biomarkers become abnormal later, and correlate with clinical symptom severity. Copyright 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                liuhua.shi@emory.edu
                Journal
                Nat Commun
                Nat Commun
                Nature Communications
                Nature Publishing Group UK (London )
                2041-1723
                19 November 2021
                19 November 2021
                2021
                : 12
                : 6754
                Affiliations
                [1 ]GRID grid.189967.8, ISNI 0000 0001 0941 6502, Gangarosa Department of Environmental Health, Rollins School of Public Health, , Emory University, ; Atlanta, GA USA
                [2 ]GRID grid.189967.8, ISNI 0000 0001 0941 6502, Department of Epidemiology, Rollins School of Public Health, , Emory University, ; Atlanta, GA USA
                [3 ]GRID grid.213917.f, ISNI 0000 0001 2097 4943, School of Earth and Atmospheric Sciences, , Georgia Institute of Technology, ; Atlanta, GA USA
                [4 ]GRID grid.189967.8, ISNI 0000 0001 0941 6502, Department of Biostatistics and Bioinformatics, Rollins School of Public Health, , Emory University, ; Atlanta, GA USA
                [5 ]GRID grid.452413.5, ISNI 0000 0001 0720 8347, School of Public Policy and Government, , Fundação Getúlio Vargas, ; Brasília, DF Brazil
                [6 ]GRID grid.34477.33, ISNI 0000000122986657, Department of Epidemiology, School of Public Health, , University of Washington, ; Seattle, WA USA
                [7 ]GRID grid.189967.8, ISNI 0000 0001 0941 6502, Department of Neurology and Human Genetics, School of Medicine, , Emory University, ; Atlanta, GA USA
                [8 ]GRID grid.38142.3c, ISNI 000000041936754X, Department of Environmental Health, , Harvard T.H. Chan School of Public Health, ; Boston, MA USA
                Author information
                http://orcid.org/0000-0001-8165-4644
                http://orcid.org/0000-0002-7564-3364
                http://orcid.org/0000-0002-7679-6282
                http://orcid.org/0000-0001-6168-378X
                Article
                27049
                10.1038/s41467-021-27049-2
                8604909
                34799599
                9ceff25f-5dad-47da-b1ad-71929bfe06a9
                © The Author(s) 2021

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 25 May 2021
                : 1 November 2021
                Funding
                Funded by: FundRef https://doi.org/10.13039/100000049, U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging);
                Award ID: R01 AG074357
                Award Recipient :
                Funded by: FundRef https://doi.org/10.13039/100006528, Emory University | Alzheimer's Disease Research Center, Emory University (Emory Alzheimer's Disease Research Center);
                Award ID: P50 AG025688
                Award Recipient :
                Funded by: FundRef https://doi.org/10.13039/100010416, Emory University | Rollins School of Public Health (RSPH);
                Award ID: P30 ES019776
                Award Recipient :
                Categories
                Article
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                © The Author(s) 2021

                Uncategorized
                alzheimer's disease,environmental impact
                Uncategorized
                alzheimer's disease, environmental impact

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