by JESSICA MOUZO
A team of scientists identifies a molecular mechanism that helps explain how airborne toxins influences Lewy body dementia
Air pollution makes people sick and can be deadly — in many ways. It has been shown to drive cardiovascular diseases, respiratory infections, and cancers such as lung cancer. It is responsible for 4.2 million premature deaths worldwide every year. There is no doubt about its harmful potential, but science is increasingly trying to pinpoint the exact links between pollution and different illnesses. A new study, published on Thursday in Science, focuses on the connection between air pollution and the risk of developing dementia, a group of neurodegenerative diseases traditionally associated with aging and characterized by the loss of memory and individual autonomy.
Specifically, researchers from Johns Hopkins University in the United States, who authored the study, focused on Lewy body dementia, a neurodegenerative disorder marked by the abnormal accumulation in the brain of a protein called alpha-synuclein. These harmful deposits (Lewy bodies), which are distinctive signs of this type of dementia and also of Parkinson’s disease, are responsible for motor problems and memory loss. And according to this new research, that protein may also hold the key to explaining how prolonged exposure to air pollution increases the risk of developing this type of dementia. The study provides scientific support for the potential of air pollutants to fuel disease and suggests that alpha-synuclein is a crucial mediator linking environmental damage to brain damage.
Xiaobo Mao, a researcher in the Department of Neurology at Johns Hopkins University and author of the study, explains that his intention was to dig deeper into a major knowledge gap — “a black box” that made it impossible to understand exactly how pollution damages the brain. The association between pollution and the risk of developing dementia had already been demonstrated, but, he notes, “the specific molecular mechanisms were not clear.”
The researchers focused specifically on Lewy body dementia because of its public health impact — it is the second most common neurodegenerative dementia, after Alzheimer’s — and because its link to pollution was “a blind spot for science,” he says, almost unknown. “We saw a pressing need to investigate whether this common environmental exposure could be a risk factor for this devastating and widespread disease,” he explains in an email response.
The first thing the scientists did was delve into epidemiological research to confirm the association already suggested by earlier scientific literature. They used data from 56 million U.S. patients hospitalized with neurodegenerative diseases between 2000 and 2014. They focused on those with Lewy body-related diseases and also calculated their exposure to fine particulate matter (PM2.5) — an airborne pollutant produced by vehicle combustion, factories, or the burning of materials. When they cross-referenced the data, the scientists found that as exposure to these environmental toxins increased, so did the risk of hospital admission for these neurodegenerative conditions.
Then, in experiments with mice, they confirmed that normal rodents exposed to these pollutants developed buildups of alpha-synuclein and ultimately suffered brain atrophy, neuronal death, and cognitive decline — all hallmarks of dementia. In contrast, when the same pollutants were given to genetically modified mice that did not produce alpha-synuclein, no significant brain changes were observed: no atrophy, no cognitive decline. “The pollution was still present, but without its key target protein, it could not cause this specific type of neurodegeneration,” the researcher adds.
The scientists’ hypothesis is that environmental toxins such as PM2.5 could trigger abnormal accumulations of alpha-synuclein capable of spreading damage throughout the brain.
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