- In a new study, researchers report that people exposed to higher levels of fine particulate air pollution had more amyloid plaques in their brains.
- Amyloid plaques are a known biomarker for Alzheimer’s disease.
- Researchers said that the correlation between pollution exposure and plaques was actually strongest among those lacking a gene variant that raises Alzheimer’s risk.
Levels of amyloid plaques and tau tangles in the brain — both key markers for Alzheimer’s disease — are elevated among people who are exposed to high levels of traffic-related air pollution.
That’s according a new study published in the journal Neurology.
“These results add to the evidence that fine particulate matter from traffic-related air pollution affects the amount of amyloid plaque in the brain,” said Anke Huels, PhD, a study author and assistant professor at Emory University in Atlanta, in a statement.
The findings also are part of a growing body of research showing the myriad ways that air pollution can have on Health in general.
Huels and her colleagues, for example, have previously
“This study really shows again that air pollution can affect every single organ in the body,” Huels told Medical News Today. “Most people know that air pollution can affect respiratory health and your lungs but are not aware about the effects on the brain and Alzheimer’s. It’s kind of scary.”
In their new study, Huels and her colleagues examined brain tissue donated by 224 people who died at an average age of 76.
They correlated the prevalence of Alzheimer’s markers found in the participants’ brains with known air pollution exposure based on their home addresses in the Atlanta area.
Researchers reported that people who were exposed to the highest levels of fine-particulate air pollution — classified as pollutant particles less than 2.5 microns in diameter — were more likely to have higher levels of amyloid plaques in their brains.
“One biological mechanism that may be involved with small particulates is that when you inhale them they can cross the blood-brain barrier and enter the brain,” Huels said. “These particles are toxic, so as soon as they reach the brain they can cause damage.”
Those who had pollution exposure that was one microgram per cubic meter (1 µg/m3) higher than average in the year before their death were nearly twice as likely to have higher levels of plaques.
Those with higher exposure in the three years before death were 87% more likely to have higher plaque levels.
The researchers reported that the strongest relationship between air pollution and amyloid plaques was among those without the gene variant APOE e4, which is known to be associated with Alzheimer’s risk.
“This suggests that environmental factors such as air pollution could be a contributing factor to Alzheimer’s in patients in which the disease cannot be explained by genetics,” Huels said.
Dr. Dale Bredesen, a neurologist as well as the senior director of Precision Brain Health at Pacific Neuroscience Institute and the chief scientific officer at Apollo Health, told Medical News Today that about 9% of people who lack the APOE e4 gene develop Alzheimer’s disease, compared to about 30% of those who have one copy of the gene in their DNA and 70% of those who have two copies of the APOE e4 gene.
Bredesen called particulate air pollution “a multiple time bad player” because it contributes to three types of “insults” to the body that can cause Alzheimer’s disease.
Those are: inflammation (which causes amyloid plaques to form); impaired blood flow, which reduces the brain’s energy supply; and toxicity, which interferes with proper brain functioning.
“There are multiple ways that pollution reduces the support of the [neural] network,” said Bredesen, who was not involved in the latest research. “There are dozens of silent Alzheimer’s killers, including sleep apnea, periodontitis, and having a leaky gut. Of currently living Americans, 45 million will die of Alzheimer’s disease because it has a lot of relatively silent contributors,” including pollution, Bredesen said.
Huels said followup studies could look to replicate the results in larger brain banks.
She noted that for this study researchers only had access to the donors last known address before they died.
“Ideally we’d like to look at lifetime exposure,” said Huels.
