Air pollution is linked to divergent cortical thickness patterns in brain regions vulnerable to Alzheimer's disease.

INTRODUCTION

Ambient air pollution increases Alzheimer's disease (AD) risk, yet exposure associations with cortical thickness (CTh) in AD-vulnerable brain regions is unclear. Here we examined the associations between PM2.5 and NO2 with CTh in an AD meta-region of interest (ROI), and across the cortex, in participants from the Vietnam Era Twin Study of Aging (VETSA) and Women's Health Initiative Memory Study (WHIMS).

METHODS

We conducted a cross-sectional study using data from 387 VETSA men (Mage=61.9 ± 2.6) and 1097 WHIMS women (Mage=77.9 ± 3.7) without dementia or stroke prior to MRI. Long-term residential exposures to PM2.5 and NO2 were quantified as the 3-year average of monthly estimates prior to MRI that were derived from spatiotemporal models with regionalized universal kriging. Brain MRI scans were processed using FreeSurfer-v.5.3.0 to estimate CTh in 34 bilateral regions parcellated with the Desikan-Killiany atlas. An AD meta-ROI was calculated as the surface-area weighted average of CTh in four bilateral regions (entorhinal, fusiform, inferior temporal, and middle temporal cortices) that are vulnerable to AD. Linear mixed models were conducted separately in each cohort with appropriate covariates.

RESULTS

In WHIMS, exposures were negatively associated with CTh in the AD meta-ROI (pPM2.5<0.001; pNO2=0.018) and diffusely across the cortex. In VETSA, exposures were positively associated with CTh in the AD meta-ROI (pPM2.5=0.017; pNO2=0.021) and temporal pole, but effects were age-dependent, becoming negative (though nonsignificant) after age 64.

DISCUSSION: Positive associations in younger VETSA men, coupled with negative associations in older WHIMS women, may suggest nonmonotonic AD-related neurodegeneration.