Air pollution and plasma amyloid beta in a cohort of older adults: Evidence from the Ginkgo Evaluation of Memory study

Hajat, Anjum; Park, Christina; Adam, Claire; Fitzpatrick, Annette L.; Ilango, Sindana D.; Leary, Cindy S.; Libby, Tanya; López, Oscar L.; Semmens, Erin O.; Kaufman, Joel D.

doi:10.1016/j.envint.2023.107800

Cited by 9 publications

(6 citation statements)

References 54 publications

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“…Further, nationally based large studies reported long-term associations between environmental pollutants and ADRD incidence. 61 , 62 Our study contributes to the literature by demonstrating an ecological association in South Carolina, a state rarely studied in neighborhood research. We also expand on the literature by demonstrating an ecological association between

and ADRD incidence stratified by race/ethnicity where NH-black populations had a stronger magnitude, although confidence intervals overlapped with results from NH-white populations.…”

Section: Discussionmentioning

confidence: 63%

Features of the Physical and Social Neighborhood Environment and Neighborhood-Level Alzheimer’s Disease and Related Dementia in South Carolina

Alhasan,

Larson,

Lohman

et al. 2024

Environ Health Perspect

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Background: Studies are increasingly examining the relationship between the neighborhood environment and cognitive decline; yet, few have investigated associations between multiple neighborhood features and Alzheimer’s disease and related dementias (ADRD). Objective: We investigated the relationship between neighborhood features and ADRD cumulative incidence from 2010 to 2014 in the South Carolina Alzheimer’s Disease Registry (SCADR). Methods: Diagnosed ADRD cases of age were ascertained from the SCADR by ZIP code and census tract. Neighborhood features from multiple secondary sources included poverty, air pollution [particulate matter with a diameter of 2.5 micrometers or less ( )], and rurality at the census-tract level and access to healthy food, recreation facilities, and diabetes screening at the county level. In addition to using Poisson generalized linear regression to estimate ADRD incident rate ratios (IRR) with 95% confidence intervals (CIs), we applied integrated nested Laplace approximations and stochastic partial differential equations (INLA-SPDE) to address disparate spatial scales. We estimated associations between neighborhood features and ADRD cumulative incidence. Results: The average annual ADRD cumulative incidence was 690 per 100,000 people per census tract (95% CI: 660, 710). The analysis was limited to 98% of census tracts with a population old (i.e., 1,081 of 1,103). The average percent of families living below the federal poverty line per census tract was 18.8%, and of census tracts were considered rural. The average percent of households with limited access to healthy food was 6.4%. In adjusted models, every ) increase of was associated with 65% higher ADRD cumulative incidence ( ; 95% CI: 1.30, 2.09), where at or below is considered healthy. Compared to large urban census tracts, rural and small urban tracts had 10% ( ; 95% CI: 1.00, 1.23) and 5% ( ; 95% CI: 0.96, 1.16) higher ADRD, respectively. For every percent increase of the county population with limited access to healthy food, ADRD was 2% higher ( ; 95% CI: 1.01, 1.04). Conclusions: Neighborhood environment features, such as higher air pollution levels, were associated with higher neighborhood ADRD incidence. The INLA-SPDE method could have broad applicability to data collected across disparate spatial scales. https://doi.org/10.1289/EHP13183

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and ADRD incidence stratified by race/ethnicity where NH-black populations had a stronger magnitude, although confidence intervals overlapped with results from NH-white populations.…”

Section: Discussionmentioning

confidence: 63%

Features of the Physical and Social Neighborhood Environment and Neighborhood-Level Alzheimer’s Disease and Related Dementia in South Carolina

Alhasan,

Larson,

Lohman

et al. 2024

Environ Health Perspect

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“…Another study found similar associations in a population composed of participants with either MCI or dementia 39 , a population that is more comparable to our own autopsy cohort, in which 71.9% were diagnosed with either AD or other forms of dementia. Limited research has explored the association between air pollution and Aβ measured in CSF or plasma, but two recent studies showed an association between PM 2.5 absorbance and CSF AD biomarkers for higher levels of brain Aβ deposition 15 as well as between PM 2.5 exposure and plasma-based measures of Aβ 40 . Therefore, our study makes an important contribution to a growing body of evidence that PM 2.5 affects Aβ deposition and neuritic plaque formation in the brain.…”

Section: Discussionmentioning

confidence: 99%

Fine particulate air pollution and neuropathology markers of Alzheimer’s disease in donors with and without APOE ε4 alleles – results from an autopsy cohort

Christensen

Liang

et al. 2023

Preprint

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Introduction: Higher fine particulate matter (PM2.5) exposure has been found to be associated with Alzheimer's disease (AD). PM2.5 has been hypothesized to cause inflammation and oxidative stress in the brain, contributing to neuropathology. A major genetic risk factor of AD, the apolipoprotein E (APOE) gene, has also been hypothesized to modify the association between PM2.5 and AD. However, little prior research exists to support these hypotheses. Therefore, this paper aims to investigate the association between traffic-related PM2.5 and AD hallmark pathology, including effect modification by APOE genotype, in an autopsy cohort. Methods: Brain tissue donors enrolled in the Emory Goizueta Alzheimer's Disease Research Center (ADRC) who died before 2020 (n=224) were assessed for AD pathology including Braak Stage, Consortium to Establish a Registry for AD (CERAD) score, and the combined AD neuropathologic change (ABC score). Traffic-related PM2.5 concentrations were modeled for the metro-Atlanta area during 2002-2019 with a spatial resolution of 200-250m. One-, 3-, and 5-year average PM2.5 concentrations prior to death were matched to participants home address. We assessed the association between traffic-related PM2.5 and AD hallmark pathology, as well as effect modification by APOE genotype, using adjusted ordinal logistic regression models. Results: Traffic-related PM2.5 was significantly associated with CERAD score for the 1-year exposure window (OR: 1.92; 95% CI: 1.12, 3.30), and the 3-year exposure window (OR: 1.87; 95%-CI: 1.01, 3.17). PM2.5 had harmful, but non-significant associations on Braak Stage and ABC score. The strongest associations between PM2.5 and neuropathology markers were among those without APOE ε4 alleles (e.g., for CERAD and 1-year exposure window, OR: 2.31; 95% CI: 1.36, 3.94), though interaction between PM2.5 and APOE genotype was not statistically significant. Conclusions: Our study found traffic-related PM2.5 exposure was associated with CERAD score in an autopsy cohort, contributing to epidemiologic evidence that PM2.5 affects Aβ deposition in the brain. This association was particularly strong among donors without APOE ε4 alleles. Future studies should further investigate the biological mechanisms behind this assocation.

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“…Animal studies have shown that air pollution exposure contributes to AD pathogenic processes such as beta-amyloid (Aβ) and tau deposition, 62 and this was supported in recent human studies using PET imaging 9 , CSF and plasma biomarkers. 10,63 Progressive exposure-related MTL atrophy may also result from neuropathological processes apart from preclinical AD, 6 such as hippocampal sclerosis, 64 primary age-related tauopathy (PART), 65 and limbic-predominant age-related TDP-43 encephalopathy (LATE). 66 Although the neuropathological processes underlying the observed associations in our study are unclear, our findings should motivate future studies that use PET and other biomarkers to test the hypothesized mediating role of Aβ or tau between exposures and MTL atrophy across different age-related neurodegenerative conditions.…”

Section: Discussionmentioning

confidence: 99%

Association between late-life air pollution exposure and medial temporal lobe atrophy in older women

Wang,

Salminen,

Petkus

et al. 2023

Preprint

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BackgroundAmbient air pollution exposures increase risk for Alzheimer’s disease (AD) and related dementias, possibly due to structural changes in the medial temporal lobe (MTL). However, existing MRI studies examining exposure effects on the MTL were cross-sectional and focused on the hippocampus, yielding mixed results.MethodTo determine whether air pollution exposures were associated with MTL atrophy over time, we conducted a longitudinal study including 653 cognitively unimpaired community-dwelling older women from the Women’s Health Initiative Memory Study with two MRI brain scans (MRI-1: 2005-6; MRI-2: 2009-10; Mageat MRI-1=77.3±3.5years). Using regionalized universal kriging models, exposures at residential locations were estimated as 3-year annual averages of fine particulate matter (PM2.5) and nitrogen dioxide (NO2) prior to MRI-1. Bilateral gray matter volumes of the hippocampus, amygdala, parahippocampal gyrus (PHG), and entorhinal cortex (ERC) were summed to operationalize the MTL. We used linear regressions to estimate exposure effects on 5-year volume changes in the MTL and its subregions, adjusting for intracranial volume, sociodemographic, lifestyle, and clinical characteristics.ResultsOn average, MTL volume decreased by 0.53±1.00cm3over 5 years. For each interquartile increase of PM2.5(3.26µg/m3) and NO2(6.77ppb), adjusted MTL volume had greater shrinkage by 0.32cm3(95%CI=[-0.43,-0.21]) and 0.12cm3(95%CI=[-0.22,-0.01]), respectively. The exposure effects did not differ byAPOEε4 genotype, sociodemographic, and cardiovascular risk factors, and remained among women with low-level PM2.5exposure. Greater PHG atrophy was associated with higher PM2.5(b=-0.24, 95%CI=[-0.29,-0.19]) and NO2exposures (b=-0.09, 95%CI=[-0.14,-0.04]). Higher exposure to PM2.5but not NO2was also associated with greater ERC atrophy. Exposures were not associated with amygdala or hippocampal atrophy.ConclusionIn summary, higher late-life PM2.5and NO2exposures were associated with greater MTL atrophy over time in cognitively unimpaired older women. The PHG and ERC - the MTL cortical subregions where AD neuropathologies likely begin, may be preferentially vulnerable to air pollution neurotoxicity.HighlightsFirst longitudinal study on air pollution and medial temporal lobe (MTL) volume.Late-life PM2.5and NO2associated with MTL atrophy over time in older women.Heterogeneous adverse effects were observed across different subregions of the MTL.Results not differ byAPOEgenotype, age, education, or cardiovascular risk factors.Adverse effects remained at low-level exposure compliant with regulatory standards.

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Air pollution and plasma amyloid beta in a cohort of older adults: Evidence from the Ginkgo Evaluation of Memory study

Cited by 9 publications

References 54 publications

Features of the Physical and Social Neighborhood Environment and Neighborhood-Level Alzheimer’s Disease and Related Dementia in South Carolina

Features of the Physical and Social Neighborhood Environment and Neighborhood-Level Alzheimer’s Disease and Related Dementia in South Carolina

Fine particulate air pollution and neuropathology markers of Alzheimer’s disease in donors with and without APOE ε4 alleles – results from an autopsy cohort

Association between late-life air pollution exposure and medial temporal lobe atrophy in older women

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