A New Link Between Air Pollution and Dementia
A major scientific study has uncovered compelling evidence that air pollution may directly increase the risk of Lewy body dementia (LBD), a group of diseases that includes Parkinson’s disease dementia (PDD) and Dementia with Lewy bodies (DLB). Previous studies have linked poor air quality to general cognitive decline, but many gaps still exist in delineating the connection between the two. This recent study, published in Science on September 4, 2025, is one of the first studies to focus specifically on LBD, which is characterized by the abnormal buildup of a protein called alpha-synuclein in the thinking parts of the brain.
Results Show Pollution-Linked Risk to LBD
This study investigated whether air pollution affects LBD risk by analyzing health records between 2000 and 2014 from 56.5 million US adults over the age of 65. Based on zip code, the study investigated levels of exposure to fine particulate matter smaller than 2.5 micrometers (PM2.5) – potentially harmful airborne particles with sources such as vehicle exhaust, wildfires, and industrial emissions. The exposure to these particles was then correlated to diagnosis of LBD.
Utilizing hospital records in different geographic areas, the study uncovered that higher long-term PM2.5 exposure was associated with a greater risk of developing LBD. For each increase in PM2.5 levels there was a 17% higher risk of PDD and a 12% higher risk of DLB.
The Biological Mechanism Behind this Link
The epidemiological data established a strong association between levels of air pollution and LBD, but to understand the mechanisms behind this link, studies were conducted in mice, exposing them to PM2.5. Normal mice that were exposed to PM2.5 over months developed brain atrophy, and cognitive deficits. However, genetically modified mice that lack alpha-synuclein did not show these changes suggesting that this protein is key to the harmful effects of pollution on the brain.
Mice bearing an αSyn A53T mutation are prone to developing αSyn aggregates and associated pathology as they age. Upon exposure to PM2.5, they developed much more widespread and toxic αSyn aggregation than the mice not exposed to PM2.5. This effect was shown not to be limited to typical US-based PM2.5 samples. PM2.5 samples were collected from China and Europe as well to reveal the same effect on the brain.
The combination of these mice studies with the large cohort of human patient analysis provides one of the most convincing molecular explanations to date for how air pollution may trigger neurodegeneration.
Implications for Public Health
This study suggests that air pollution is a major public health concern that may contribute to the development of LBD. PM2.5 can be reduced and/or limited by the use of cleaner energy sources, tighter emissions standards, and personal choices like indoor air filtration.
Further research is needed to pinpoint the most harmful components of air pollution to understand how they trigger these diseases and what can be done to prevent them, but this study stresses the urgency for action to be taken sooner rather than later.
Environmental links to PD have focused up until this point mainly on exposure to pesticides and solvents, not air pollution. This current study demonstrates that the search for environmental links to PD must be much broader to fully encapsulate and address all the potential risks.
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