Air Pollution Increases Dementia Risk Among Older Women

by Dr. Meenakshy Varier on  February 1, 2017 at 2:40 PM Health Watch
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Highlights
  • Apolipoprotein E (APOE) is a genetic variant that increases the risk of Alzheimer's disease or AD.
  • Study shows that in people who have this genetic variant, exposure to particulate matter (PM) in the ambient air accelerates the process of dementia, including Alzheimer's disease.
  • These particles gain entry through the nose into the brain, which triggers inflammatory responses and over the course of time promotes risk of Alzheimer's disease.
Tiny air pollution particles that mainly comes from power plants and automobiles, may greatly increase the chance of dementia, including Alzheimer's disease.
Air Pollution Increases Dementia Risk Among Older Women
Air Pollution Increases Dementia Risk Among Older Women

The findings are according to research led by University of Southern California, (USC)..

The study found that older women who live in places with exposure to fine particulate matter that exceeds the U.S. Environmental Protection Agency's standard are 81% more at risk for global cognitive decline and 92% more likely to develop dementia, including Alzheimer's disease.

According to the World Health Organization, nearly 48 million people suffer from dementia, and there are 7.7 million new cases annually, worldwide.

Role of Pollutants

Apolipoprotein E (APOE) is a genetic variant that increases the risk for AD but all inheritable causes account for only 50% of the risk for AD.

Environmental influences on Alzheimer's disease (AD) and related dementia are poorly documented.

So, it is necessary to identify the role of environmental risk factors, including common neurotoxins and their interactions with Apolipoprotein E (APOE) and other genes.

Ambient fine particulate matter or PM2.5 are fine, inhalable particles with diameters of 2.5 micrometers or smaller. These are emitted mainly from traffic and are a major source of urban air pollution, accounting globally for 25% of ambient PM.

Among the elderly, epidemiological evidence associates cognitive deficits with PM2.5 exposure.

According to the study, in the general population, air pollution could be responsible for about 21% of dementia cases.

"Microscopic particles generated by fossil fuels get into our body directly through the nose into the brain," said University Professor Caleb Finch at the USC Leonard Davis School of Gerontology and co-senior author of the study. "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 added.

The adverse effects were prominent in women who had the APOE4 gene.

"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," said Jiu-Chiuan Chen, co-senior author of the study and an associate professor of preventive medicine at the Keck School of Medicine of USC.

"The experimental data showed that exposure of mice to air particles collected on the edge of USC damaged neurons in the hippocampus, the memory center that is vulnerable to both brain aging and Alzheimer's disease." Chen added.

Study Involving Women and Mice

The researchers analyzed data of 3,647 women aged 65-79 years from the Women's Health Initiative Memory Study (WHIMS).

These women were free of dementia when they had enrolled for the study and lived across 48 states.

The technology to collect air particles for controlled exposure of mouse models, was invented by Constantinos Sioutas, the Fred Champion Professor of Civil and Environmental Engineering at USC Viterbi.

"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 Sioutas, co-author of the study. "We then use these samples to test exposure and assess adverse neuro-developmental or neuro-degenerative health effects."

Researchers then exposed female mice carrying the APOE4 gene, who were predisposed to Alzheimer's disease, to nano-sized air pollution chronically for 15 weeks.

The mice exposed to pollutants accumulated as much as 60% more amyloid plaques. These plaques are toxic clusters of protein fragments that cause the progression of Alzheimer's.

"Our study has global implications as pollution knows no borders," said Finch.

"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."

Conclusion

The researchers found that by reducing PM2.5 in the air the number of cases of dementia can be reduced.

"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."

More research is needed to confirm a causal relationship and to understand how air pollution enters the brain and triggers harmful reactions.

The limitation of the study is that it examined only women and female mice.

In future, researchers plan to include both sexes to evaluate the effect on men and to examine the interaction of PM2.5 with cigarettes and other pollutants.

The study conducted in collaboration between USC Davis, the Keck School of Medicine and the USC Viterbi School of Engineering is published in the Nature journal Translational Psychiatry.

Reference

  1. Caleb Finch et al. Particulate air pollutants, APOE alleles and their contributions to cognitive impairment in older women and to amyloidogenesis in experimental models. Translational Psychiatry ; (2017) doi:10.1038/tp.2016.280


Source: Medindia

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