Interaction Between Air Pollution, Genetics May Create Significant Risk of Alzheimer’s

Interaction Between Air Pollution, Genetics May Create Significant Risk of Alzheimer’s

High levels of air pollution particles may increase the risk of dementia and Alzheimer’s disease in older women, according to results of a new study.

These particles, found in emissions from power plants and cars, increase the risk of dementia, including Alzheimer’s, by as much as 92%, especially in women with the ApoE4 gene variant, which has been associated with this disease.

These findings also may have serious implications for the general population, as pollution is one of the world’s most profound issues. Researchers said pollution may account for nearly 21% of dementia cases.

Results of the study were published in the journal Translational Psychiatry with the title “Particulate Air Pollutants, APOE Alleles And Their Contributions To Cognitive Impairment In Older Women And To Amyloidogenesis In Experimental Models.

“Microscopic particles generated by fossil fuels get into our body directly through the nose into the brain,” Caleb Finch, PhD, one of the study’s senior authors, explained in a press release. “Cells in the brain treat these particles as invaders and react with inflammatory responses, which over the course of time appear to exacerbate and promote Alzheimer’s disease.

“Although the link between air pollution and Alzheimer’s disease is a new scientific frontier, we now have evidence that air pollution, like tobacco, is dangerous to the aging brain,” Finch said.

Researchers studied the interaction between air pollution and genetics by analyzing data from 3,647 women (65 to 79 years old) included in the Women’s Health Initiative Memory Study (WHIMS). These women lived across the U.S. and didn’t have dementia before the study.

Results indicated that women living in places where pollution exceeds the standard levels of the U.S. Environmental Protection Agency had a higher risk of cognitive decline (81%) and dementia (92%). These effects were stronger in women who also had the ApoE4 gene variant.

Researchers also observed that female mice with the ApoE4 variant that were exposed to air pollution for 15 weeks had 60% more accumulation of beta-amyloid, the protein that becomes toxic in Alzheimer’s disease.

“Our study — the first of its kind conducted in the U.S. — provides the inaugural scientific evidence of a critical Alzheimer’s risk gene possibly interacting with air particles to accelerate brain aging,” Jiu-Chiuan Chen, MD, the study’s other senior author, said. “The experimental data showed that exposure of mice to air particles … damaged neurons in the hippocampus, the memory center that is vulnerable to both brain aging and Alzheimer’s disease.”

The study also identified the air pollutants responsible for these damaging effects as small, inhalable particles known as PM2.5. The exposure experiments in female mice were carried out using a technology that collects air particles.

“Our state-of-the-art aerosol technologies, called particle concentrators, essentially take the air of a typical urban area and convert it to the air of a freeway or a heavily polluted city like Beijing,” said Constantinos Sioutas, inventor of the technology. “We then use these samples to test exposure and assess adverse neuro-developmental or neuro-degenerative health effects,” he said.

The values of excessive PM2.5 used in the study come from data collected from pollution monitors. However, according to the American Lung Association, less than one-third of all American counties have such technology for pollution control.

“We analyzed data of high PM2.5 levels using standards the EPA set in 2012,” Chen said. “We don’t know whether the lower PM2.5 levels of recent years have provided a safe margin for older Americans, especially those at risk for dementia.”

Six of the 10 most polluted cities in the U.S. are in California, including Los Angeles, Long Beach and Fresno, and more cities are becoming gradually more polluted. Researchers believe that reduced PM2.5 levels in the air are associated with fewer cases of dementia.

“Many studies have suggested that early life adversities may carry into later life and affect brain aging,” Chen said. “If this is true, then maybe long-term exposure to air pollution that starts a downward spiral of neurodegenerative change in the brain could begin much earlier and rev up in later life.”

The team has also found that prolonged exposure to high PM2.5 levels led to loss of gray and white matter volumes in brain regions that process thinking, decision-making and planning.

More studies are warranted with people from both genders to investigate whether air pollution also may affect men, and whether PM2.5 interacts with cigarettes and other pollutants.

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