{"id":10660,"date":"2026-08-18T06:00:00","date_gmt":"2026-08-18T13:00:00","guid":{"rendered":"https:\/\/keck.usc.edu\/news\/?p=10660"},"modified":"2026-08-20T09:28:47","modified_gmt":"2026-08-20T16:28:47","slug":"air-pollution-linked-to-distinct-brain-changes-in-regions-vulnerable-to-alzheimers-disease","status":"publish","type":"post","link":"https:\/\/keck.usc.edu\/news\/air-pollution-linked-to-distinct-brain-changes-in-regions-vulnerable-to-alzheimers-disease\/","title":{"rendered":"Air pollution linked to distinct brain changes in regions vulnerable to Alzheimer\u2019s disease"},"content":{"rendered":"\n

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Air pollution linked to distinct brain changes in regions vulnerable to Alzheimer\u2019s disease<\/h1>\n\n\n<\/div>\n \n \n
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USC researchers found that exposure to common air pollutants was associated with different patterns of cortical thickness in two groups of older adults, pointing to a potentially complex relationship between pollution, aging, and brain health.<\/p>\n\n\n\n<\/div>\n \n

\n Sidney Taiko Sheehan<\/span>\n \n August 18, 2026<\/span>\n <\/div>\n \n \n
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Brain maps show how exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) was associated with cortical thickness in two groups of older adults.\u00a0Warmer\u00a0colors indicate regions where greater exposure was linked to a\u00a0thinner\u00a0cortex (in WHIMS), while\u00a0cooler\u00a0colors indicate regions where greater exposure was linked to a\u00a0thicker\u00a0cortex (in VETSA). Photo\/Stevens INI<\/p>\n<\/figcaption>\n <\/figure>\n \n \n \n\n<\/div>\n \n\n <\/div><\/div>\n\n\n\n\n \n \n\n\n\n\n\n\n\n

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Exposure to common forms of outdoor air pollution may be linked to structural changes in brain regions that are especially vulnerable to Alzheimer\u2019s disease, according to a new study led by researchers from the USC Mark and Mary Stevens Neuroimaging and Informatics Institute (<\/span>Stevens INI<\/span><\/a>) at the Keck School of Medicine of USC.<\/span><\/p>\n

The study, <\/span>published in NeuroToxicology<\/span><\/a>, examined brain scans and residential air pollution estimates from 1,484 adults without dementia or a history of stroke. In a group of older women, greater exposure to fine particulate matter and nitrogen dioxide was associated with a thinner cortex, the brain\u2019s outer layer, in regions important for memory and commonly affected by Alzheimer\u2019s disease.<\/span><\/p>\n

The researchers found an unexpectedly different pattern among a separate group of younger men: Greater pollution exposure was associated with a thicker cortex in the same Alzheimer\u2019s-vulnerable regions. That association weakened with age and reversed around age 65, although the later negative association was not statistically significant.<\/span><\/p>\n

The divergent findings may reflect different phases of a complex biological response to pollution, but the researchers caution that the study cannot determine whether age, sex, or other differences between the two groups account for the results.<\/span><\/p>\n

\u201cAir pollution did not correspond to one uniform pattern of brain structure across all participants,\u201d said <\/span>Lauren Salminen, PhD<\/span><\/a>, lead author of the study and assistant professor of research neurology. \u201cThe contrasting findings suggest that the brain\u2019s response to pollution may change across the aging process. Following people over time will be essential for determining what these patterns mean for Alzheimer\u2019s risk.\u201d<\/span><\/p>\n

Measuring pollution\u2019s imprint on the brain<\/b><\/h2>\n

The researchers studied two independent groups: 387 men from the Vietnam Era Twin Study of Aging, who were about 62 years old on average, and 1,097 women from the Women\u2019s Health Initiative Memory Study, whose average age was approximately 78.<\/span><\/p>\n

Using participants\u2019 residential histories, the team estimated exposure during the three years before each person\u2019s MRI scan to two widespread outdoor air pollutants: fine particulate matter, known as PM2.5, and nitrogen dioxide, or NO2.<\/span><\/p>\n

PM2.5 consists of particles less than 2.5 micrometers wide\u2014small enough to travel deep into the lungs and potentially enter the bloodstream. It can come from vehicle exhaust, power plants, wildfires, and other sources of combustion. NO2 is a gas produced largely by burning fossil fuels and is commonly associated with traffic.<\/span><\/p>\n

The researchers then measured cortical thickness across the brain. The cortex is the folded outer layer involved in memory, language, decision-making, and many other essential functions. It generally becomes thinner with age, and accelerated thinning in certain regions can be a sign of neurodegeneration.<\/span><\/p>\n

The team focused first on four areas that are particularly vulnerable to Alzheimer\u2019s disease: the entorhinal, fusiform, inferior temporal, and middle temporal cortices. Together, these regions formed a combined measure of cortical thickness.<\/span><\/p>\n

Among the older women, higher exposure to both pollutants was associated with a thinner cortex in this Alzheimer\u2019s-vulnerable group of regions. For each additional microgram per cubic meter of PM2.5 exposure, the estimated difference in cortical thickness was comparable to about 13 months of aging. For each additional part per billion of NO2, the difference was comparable to roughly three months of aging.<\/span><\/p>\n

The pattern also extended well beyond regions associated with Alzheimer\u2019s. Higher PM2.5 exposure was linked to thinner cortex in 23 of the 34 brain regions examined, spanning all four lobes of the brain.<\/span><\/p>\n

Why a thicker cortex may not always mean a healthier brain<\/b><\/h2>\n

In the younger group of men, higher pollution exposure was associated with a thicker cortex in regions vulnerable to Alzheimer\u2019s disease. Although thickness is often interpreted as a sign of healthier tissue, emerging research suggests that the cortex may temporarily thicken during the earliest stages of some disease processes before becoming thinner as neurodegeneration advances.<\/span><\/p>\n

Possible explanations include inflammation, swelling or enlargement of brain cells, or early changes associated with the accumulation of amyloid, a protein involved in Alzheimer\u2019s disease. The new study did not measure amyloid, tau, or inflammation, however, so it cannot confirm whether any of these processes explain the findings.<\/span><\/p>\n

The age-related pattern among the men offers a clue: The association between PM2.5 and greater cortical thickness gradually diminished between ages 55 and 64 and became negative after approximately age 65.<\/span><\/p>\n

\u201cOur findings raise the possibility that pollution-related brain changes are not linear,\u201d Salminen said. \u201cA thicker cortex at one point in life could represent an early biological response, while thinning later in life could reflect accumulated damage. This is an important hypothesis, but it must be tested in studies that track the same people as they age and include Alzheimer\u2019s biomarkers.\u201d<\/span><\/p>\n

Because the two study groups differed in both age and sex, the researchers cannot determine which factor\u2014or combination of factors\u2014explains the contrasting results. The analysis also provides a snapshot at one point in time, meaning it cannot establish that air pollution caused the observed brain differences.<\/span><\/p>\n

Still, the findings add to evidence that environmental exposures may play a meaningful role in brain aging and dementia risk.<\/span><\/p>\n

\u201cAir pollution is a widespread and potentially modifiable risk factor that affects people across entire communities,\u201d said Arthur W. Toga, PhD, director of the Stevens INI. \u201cAdvanced brain imaging gives us a powerful way to investigate how these exposures may influence the brain long before dementia symptoms appear. Understanding when these changes begin and how they evolve could ultimately help guide more effective approaches to protecting brain health.\u201d<\/span><\/p>\n

Future research will need to follow men and women from the same study over time while measuring inflammation, amyloid, tau, and cognitive change. That could help researchers determine whether the contrasting cortical patterns represent different stages of pollution-related brain injury and whether they predict a greater risk of Alzheimer\u2019s disease.<\/span><\/p>\n

About the study<\/b><\/h2>\n

In addition to Salminen, the study\u2019s authors are Xinhui Wang, Andrew J. Petkus, Christine Fennema-Notestine, Jeremy A. Elman, Donald J. Hagler Jr., Joel D. Kaufman, Joshua Millstein, Meredith N. Braskie, Joshua Liu, Hyung Jin Cho, Deydeep Kothapalli, Paul M. Thompson, Daniel P. Beavers, Mark A. Espeland, Margaret Gatz, Susan M. Resnick, Ira Frahmand, Stephen R. Rapp, Caleb E. Finch, Jiu-Chiuan Chen, William S. Kremen, and Carol E. Franz.<\/span><\/p>\n

The research was supported by the National Institutes of Health, including the National Institute on Aging, National Institute of Environmental Health Sciences, and National Heart, Lung, and Blood Institute; the Southern California Environmental Health Sciences Center; the Alzheimer\u2019s Disease Research Center at USC; the Wake Forest Alzheimer\u2019s Disease Research Center; the NIH Intramural Research Program; and U.S. Environmental Protection Agency research assistance agreements supporting the air pollution models.<\/span><\/p>\n\n\n\n<\/div>\n <\/div>\n\n\n 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