Summary: Older women exposed to higher levels of air pollution were more likely to experience greater memory decline and Alzheimer’s-like brain atrophy compared with those exposed to cleaner air.
Women in their 70s and 80s who were exposed to higher levels of air pollution experienced greater declines in memory and more Alzheimer’s-like brain atrophy than their counterparts who breathed cleaner air, according to USC researchers.
The findings of the nationwide study, published today in Brain, touch on the renewed interest in preventing Alzheimer’s disease by reducing risk as well as hint at a potential disease mechanism. Alzheimer’s is the sixth-leading cause of death in the United States, and there’s currently no cure or treatment.
“This is the first study to really show, in a statistical model, that air pollution was associated with changes in people’s brains and that those changes were then connected with declines in memory performance,” said Andrew Petkus, assistant professor of clinical neurology at the Keck School of Medicine at USC.
“Our hope is that by better understanding the underlying brain changes caused by air pollution, researchers will be able to develop interventions to help people with or at risk for cognitive decline.”
Fine particles, also called PM2.5 particles, are about 1/30th the width of a human hair. They come from traffic exhaust, smoke and dust and their tiny size allows them to remain airborne for long periods, get inside buildings, be inhaled easily, and reach and accumulate in the brain. Fine particle pollution is associated with asthma, cardiovascular disease, lung disease and premature death.
Previous research has suggested that fine particle pollution exposure increases the risk for Alzheimer’s disease and related dementias. What scientists haven’t known is whether PM2.5 alters brain structure and accelerates memory decline.
For this study, researchers used data from 998 women, aged 73 to 87, who had up to two brain scans five years apart as part of the landmark Women’s Health Initiative. The Women’s Health Initiative was launched in 1993 by the National Institutes of Health and enrolled more than 160,000 women to address questions about heart disease, cancer and osteoporosis.
Those brain scans were scored on the basis of their similarity to Alzheimer’s disease patterns by a machine learning tool that had been “trained” via brain scans of people with Alzheimer’s disease. The researchers also gathered information about where the 998 women lived, as well as environmental data from those locations to estimate their exposure to fine particle pollution.
When all that information was combined, researchers could see the association between higher pollution exposure, brain changes and memory problems — even after adjusting to take into account differences in income, education, race, geographic region, cigarette smoking and other factors.
“This study provides another piece of the Alzheimer’s disease puzzle by identifying some of the brain changes linking air pollution and memory decline. Each research study gets us one step closer to solving the Alzheimer’s disease epidemic,” Petkus said.
In addition to Petkus, the study authors are Diana Younan, Xinhui Wang, Margaret Gatz, Helena Chui and Jiu-Chiuan Chen of USC; Keith Widaman of UC Riverside; Ramon Casanova, Mark Espeland, Stephen Rapp, Bonnie Sachs, Sarah Gaussoin, Ryan Barnard, Santiago Saldana, Daniel Beavers and Sally Shumaker of Wake Forest School of Medicine; Victor Henderson of Stanford; JoAnn Manson and Joel Salinas of Harvard Medical School; Marc Serre and William Vizuete of the University of North Carolina; and Susan Resnick of the National Institute on Aging.
Funding: The study was supported by the National Institute of Environmental Health Sciences (R01ES025888), the National Institute on Aging (R01AG033078, R21AG051113, R01AG033078, RF1AG054068 and RF1AG054068), the Southern California Environmental Health (5P30ES007048), the National Institutes of Health (P50AG047366, P50AG05142).
Leigh Hopper – USC
The image is credited to USC.
Original Research: Closed access
“Particulate matter and episodic memory decline mediated by early neuroanatomic biomarkers of Alzheimer’s disease “. Andrew Petkus et al.
Particulate matter and episodic memory decline mediated by early neuroanatomic biomarkers of Alzheimer’s disease
Evidence suggests exposure to particulate matter with aerodynamic diameter <2.5 μm (PM2.5) may increase the risk for Alzheimer’s disease and related dementias. Whether PM2.5 alters brain structure and accelerates the preclinical neuropsychological processes remains unknown. Early decline of episodic memory is detectable in preclinical Alzheimer’s disease. Therefore, we conducted a longitudinal study to examine whether PM2.5 affects the episodic memory decline, and also explored the potential mediating role of increased neuroanatomic risk of Alzheimer’s disease associated with exposure. Participants included older females (n = 998; aged 73–87) enrolled in both the Women’s Health Initiative Study of Cognitive Aging and the Women’s Health Initiative Memory Study of Magnetic Resonance Imaging, with annual (1999–2010) episodic memory assessment by the California Verbal Learning Test, including measures of immediate free recall/new learning (List A Trials 1–3; List B) and delayed free recall (short- and long-delay), and up to two brain scans (MRI-1: 2005–06; MRI-2: 2009–10). Subjects were assigned Alzheimer’s disease pattern similarity scores (a brain-MRI measured neuroanatomical risk for Alzheimer’s disease), developed by supervised machine learning and validated with data from the Alzheimer’s Disease Neuroimaging Initiative. Based on residential histories and environmental data on air monitoring and simulated atmospheric chemistry, we used a spatiotemporal model to estimate 3-year average PM2.5 exposure preceding MRI-1. In multilevel structural equation models, PM2.5 was associated with greater declines in immediate recall and new learning, but no association was found with decline in delayed-recall or composite scores. For each interquartile increment (2.81 μg/m3) of PM2.5, the annual decline rate was significantly accelerated by 19.3% [95% confidence interval (CI) = 1.9% to 36.2%] for Trials 1–3 and 14.8% (4.4% to 24.9%) for List B performance, adjusting for multiple potential confounders. Long-term PM2.5 exposure was associated with increased Alzheimer’s disease pattern similarity scores, which accounted for 22.6% (95% CI: 1% to 68.9%) and 10.7% (95% CI: 1.0% to 30.3%) of the total adverse PM2.5 effects on Trials 1–3 and List B, respectively. The observed associations remained after excluding incident cases of dementia and stroke during the follow-up, or further adjusting for small-vessel ischaemic disease volumes. Our findings illustrate the continuum of PM2.5 neurotoxicity that contributes to early decline of immediate free recall/new learning at the preclinical stage, which is mediated by progressive atrophy of grey matter indicative of increased Alzheimer’s disease risk, independent of cerebrovascular damage.