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Increased neuroanatomic risk for Alzheimer’s disease at preclinical stage: Exploring the interaction of fine particle exposure and psychosocial stress
Author(s) -
Younan Diana,
Wang Xinhui,
Petkus Andrew J,
Gruenewald Tara L,
Casanova Ramon,
Serre Marc,
Vizuete William,
Beavers Daniel P,
Braskie Meredith N,
He Ka,
Woods Nancy,
Garcia Lorena,
Wallace Robert B,
Resnick Susan M,
Manson JoAnn E,
Gatz Margaret,
Chui Helena C,
Espeland Mark A,
Chen JiuChiuan
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.046623
Subject(s) - psychosocial , medicine , sleep disorder , dementia , psychology , clinical psychology , psychiatry , disease , insomnia
Background Ambient air pollution, especially fine particulate matter (aerodynamic diameter <2.5 μm; PM 2.5 ), is a novel neurotoxin. Psychosocial stress has been linked to Alzheimer’s disease (AD) and other dementias (ADRD). We test the hypothesis that PM 2.5 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 PM 2.5 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 PM 2.5 and AD‐PS scores (5‐year standardized difference) using generalized linear models. Result Among 542 women, PM 2.5 (per 2.87 µg/m 3 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 PM 2.5 , 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 (p interaction =0.06) and among women reporting high (β=0.040; p=0.003) vs. low (β=0.005; p=0.702) sleep disturbance (p interaction =0.04). There was no evidence of effect modification by sleep duration. Conclusion Our novel findings suggest psychosocial stress may increase susceptibility to PM 2.5 neurotoxicity based on neuroanatomic AD risk at the preclinical stage. Psychosocial stress may lower the brain’s threshold to neurotoxicity, further accelerating the PM 2.5 ‐induced neurodegeneration.