Abstract
Increased neuroanatomic risk for Alzheimer’s disease at preclinical stage: Exploring the interaction of fine particle exposure and psychosocial stress
Alzheimer's & dementia, Vol.16, p.n/a
12/2020
DOI: 10.1002/alz.046623
Abstract
Background
Ambient air pollution, especially fine particulate matter (aerodynamic diameter <2.5 μm; PM2.5), is a novel neurotoxin. Psychosocial stress has been linked to Alzheimer’s disease (AD) and other dementias (ADRD). We test the hypothesis that PM2.5 and psychosocial stress may interact to accelerate brain aging, by investigating their potential joint effects on neuroanatomic risk for AD.
Method
Community‐dwelling older women (aged 71‐89) from the Women’s Health Initiative (WHI) Memory Study of MRI completed two structural brain MRI scans (MRI‐1: 2005‐6; MRI‐2: 2010‐11). To focus on the preclinical stage, we excluded women who developed MCI or dementia over follow‐up. The AD pattern similarity (AD‐PS) score, developed by supervised machine learning and validated with the AD Neuroimaging Initiative data, was used to determine the degree of high‐dimensional gray matter atrophy in brain areas vulnerable to AD. Residential three‐year average PM2.5 exposure preceding MRI‐1 were aggregated from daily estimates, based on nationwide spatiotemporal modeling. A structured questionnaire was administered to gather information on the frequency of stressful life events (SLEs) and self‐reported sleep duration. Sleep disturbance was measured using the WHI Insomnia Rating Scale, with higher numbers indicating greater insomnia. We examined whether the source (frequency of SLEs) or behavioral manifestation (sleep disturbance; sleep duration) of psychosocial stress modified the association between PM2.5 and AD‐PS scores (5‐year standardized difference) using generalized linear models.
Result
Among 542 women, PM2.5 (per 2.87 µg/m3 increase) was significantly associated with increased AD‐PS scores (β=0.020; p=0.028), adjusting for geographic region, age, socioeconomic status, lifestyle, clinical characteristics, hormone therapy use, and intracranial volume. This negative association with PM2.5, equivalent to a 7% increase in the relative risk for ADRD, was greater among women reporting high (β=0.041; p=0.004) vs. low (β=0.008; p=0.460) frequencies of SLEs (pinteraction=0.06) and among women reporting high (β=0.040; p=0.003) vs. low (β=0.005; p=0.702) sleep disturbance (pinteraction=0.04). There was no evidence of effect modification by sleep duration.
Conclusion
Our novel findings suggest psychosocial stress may increase susceptibility to PM2.5 neurotoxicity based on neuroanatomic AD risk at the preclinical stage. Psychosocial stress may lower the brain’s threshold to neurotoxicity, further accelerating the PM2.5‐induced neurodegeneration.
Details
- Title: Subtitle
- Increased neuroanatomic risk for Alzheimer’s disease at preclinical stage: Exploring the interaction of fine particle exposure and psychosocial stress
- Creators
- Diana Younan - University of Southern CaliforniaXinhui Wang - University of Southern CaliforniaAndrew J Petkus - University of Southern CaliforniaTara L Gruenewald - Chapman UniversityRamon Casanova - Wake Forest UniversityMarc Serre - University of North Carolina at Chapel HillWilliam Vizuete - University of North Carolina at Chapel HillDaniel P Beavers - Wake Forest UniversityMeredith N Braskie - University of Southern CaliforniaKa He - Columbia UniversityNancy Woods - University of WashingtonLorena Garcia - University of California, DavisRobert B Wallace - University of IowaSusan M Resnick - National Institute on AgingJoAnn E Manson - Brigham and Women's HospitalMargaret Gatz - University of Southern CaliforniaHelena C Chui - University of Southern CaliforniaMark A Espeland - Wake Forest UniversityJiu‐Chiuan Chen - University of Southern California
- Resource Type
- Abstract
- Publication Details
- Alzheimer's & dementia, Vol.16, p.n/a
- DOI
- 10.1002/alz.046623
- ISSN
- 1552-5260
- eISSN
- 1552-5279
- Number of pages
- 1
- Language
- English
- Date published
- 12/2020
- Academic Unit
- Epidemiology; Injury Prevention Research Center; Internal Medicine
- Record Identifier
- 9984364656402771
Metrics
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