RT Journal Article
SR Electronic
T1 PM<sub>2.5</sub> Associated With Gray Matter Atrophy Reflecting Increased Alzheimer Risk in Older Women
JF Neurology
JO Neurology
FD Lippincott Williams &amp; Wilkins
SP e1190
OP e1201
DO 10.1212/WNL.0000000000011149
VO 96
IS 8
A1 Younan, Diana
A1 Wang, Xinhui
A1 Casanova, Ramon
A1 Barnard, Ryan
A1 Gaussoin, Sarah A.
A1 Saldana, Santiago
A1 Petkus, Andrew J.
A1 Beavers, Daniel P.
A1 Resnick, Susan M.
A1 Manson, JoAnn E.
A1 Serre, Marc L.
A1 Vizuete, William
A1 Henderson, Victor W.
A1 Sachs, Bonnie C.
A1 Salinas, Joel
A1 Gatz, Margaret
A1 Espeland, Mark A.
A1 Chui, Helena C.
A1 Shumaker, Sally A.
A1 Rapp, Stephen R.
A1 Chen, Jiu-Chiuan
A1 ,
YR 2021
UL http://n.neurology.org/content/96/8/e1190.abstract
AB Objective To examine whether late-life exposure to PM2.5 (particulate matter with aerodynamic diameters &lt;2.5 µm) contributes to progressive brain atrophy predictive of Alzheimer disease (AD) using a community-dwelling cohort of women (age 70–89 years) with up to 2 brain MRI scans (MRI-1, 2005–2006; MRI-2, 2010–2011).Methods AD pattern similarity (AD-PS) scores, developed by supervised machine learning and validated with MRI data from the Alzheimer’s Disease Neuroimaging Initiative, were used to capture high-dimensional gray matter atrophy in brain areas vulnerable to AD (e.g., amygdala, hippocampus, parahippocampal gyrus, thalamus, inferior temporal lobe areas, and midbrain). Using participants' addresses and air monitoring data, we implemented a spatiotemporal model to estimate 3-year average exposure to PM2.5 preceding MRI-1. General linear models were used to examine the association between PM2.5 and AD-PS scores (baseline and 5-year standardized change), accounting for potential confounders and white matter lesion volumes.Results For 1,365 women 77.9 ± 3.7 years of age in 2005 to 2006, there was no association between PM2.5 and baseline AD-PS score in cross-sectional analyses (β = −0.004; 95% confidence interval [CI] −0.019 to 0.011). Longitudinally, each interquartile range increase of PM2.5 (2.82 µg/m3) was associated with increased AD-PS scores during the follow-up, equivalent to a 24% (hazard ratio 1.24, 95% CI 1.14–1.34) increase in AD risk over 5 years (n = 712, age 77.4 ± 3.5 years). This association remained after adjustment for sociodemographics, intracranial volume, lifestyle, clinical characteristics, and white matter lesions and was present with levels below US regulatory standards (&lt;12 µg/m3).Conclusions Late-life exposure to PM2.5 is associated with increased neuroanatomic risk of AD, which may not be explained by available indicators of cerebrovascular damage.AD=Alzheimer disease; ADNI=Alzheimer's Disease Neuroimaging Initiative; AD-PS=AD pattern similarity; BME=Bayesian Maximum Entropy; BMI=body mass index; CI=confidence interval; CTM=chemical transport model; EN-RLR=elastic net regularized logistic regression; EPA=Environmental Protection Agency; GLM=general linear model; ICV=intracranial volume; IQR=interquartile range; PM2.5=particulate matter with aerodynamic diameters &lt;2.5 µm; WHIMS=Women's Health Initiative Memory Study