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People with high exposure to traffic-related air pollution are more likely to have high levels of amyloid plaques in their brains, which are linked to Alzheimer’s disease, a study has found.
The study, published in the online issue of Neurology, does not prove that air pollution causes more amyloid plaques in the brain. It shows only one association.
Researchers at Emory University in Georgia, US, examined brain tissue from 224 people who had agreed to donate their brains at death to advance dementia research. People died at an average age of 76.
They looked at traffic-related air pollution exposure based on people’s home addresses in the Atlanta area at the time of death.
The average level of exposure was 1.32 micrograms per cubic meter in the year before death and 1.35 micrograms per cubic meter in the three years before death.
The researchers then compared the pollution exposure to measures of Alzheimer’s disease symptoms in the brain: amyloid plaques and tau tangles.
They found that those with higher exposure to air pollution one or three years before death were more likely to have higher levels of amyloid plaques in their brains.
Exposure to PM 2.5 greater than 1 microgram per cubic meter in the year before death was almost twice as likely, while those with higher exposure in the three years before death were 87 percent more likely to have higher levels. plaque
“These findings add to the evidence that fine particulate matter from traffic-related air pollution affects the amount of amyloid plaques in the brain,” said Emory University’s Anke Huels.
“Further research is needed to investigate the mechanisms behind this link.”
Further, the researchers also looked at whether the main gene variant associated with Alzheimer’s disease, APOE e4, had any effect on the relationship between air pollution and Alzheimer’s symptoms in the brain.
They found that the strongest association between air pollution and Alzheimer’s symptoms was without the gene variant.
“This suggests that environmental factors such as air pollution may be a contributing factor to Alzheimer’s in patients where the disease cannot be explained by genetics,” Huels said.
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