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Alzheimer’s, what is the role of air pollution?

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Alzheimer’s, what is the role of air pollution?

Pollution, how bad are you doing? There are hundreds of studies that demonstrate how living in areas with high levels of atmospheric particulate matter (the famous fine dust) exposes you to a greater risk of respiratory and cardiovascular diseases. And what do we know about the brain? Recent investigations had already linked air pollution with marked neuroinflammation profiles, and now a new study just published in Neurologythe medical journal of the American Academy of Neurology, has highlighted an association between exposure to high levels of PM 2.5 and Alzheimer’s disease.

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Pollution and amyloid plaques

The team from Emory University (Atlanta, USA) that conducted the investigation examined the brain tissue of 224 deceased people (who had previously expressed the desire to donate their brains for research purposes after death) to identify the typical signs of Alzheimer’s disease, i.e. amyloid plaques and Tau protein aggregates. These results were then compared with the levels of atmospheric particulate matter PM 2.5 recorded in the year and three years preceding the death of the people involved in the study in the area of ​​their last residence.

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In this way the researchers were able to ascertain an association between high levels of PM 2.5 and a greater number of signs of neurodegeneration. In particular, people with exposure greater than 1 µg/m3 to PM 2.5 in the year before death were almost twice as likely to have higher plaque levels, while those with greater exposure in the three years before of death were 87% more likely.

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It’s not all. The scientists also wanted to examine a possible effect of the main genetic variant linked to the development of Alzheimer’s disease (ApoE e4), discovering that the association between pollution and the presence of amyloid plaques and Tau aggregates was stronger in people who did not possess this variant genetics. “This suggests that environmental factors such as air pollution could contribute to Alzheimer’s in patients where the disease cannot be explained by genetics,” commented Anke Huels, one of the authors of the work.

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Let’s not talk about cause and effect

As the authors of the research themselves underline, what has been identified is an association. The study, in other words, does not prove that exposure to high levels of air pollution causes the formation of more amyloid plaques. A possible pathogenetic mechanism must be demonstrated with studies to this.

Furthermore, the research suffers from some limitations. The experts relied on the last available residential address of the people who donated their tissues to recover the air pollution values, but, since they were unable to confirm this, it is possible that the exposure was classified incorrectly. Finally, it should be considered that the sample of population involved is quite homogeneous, made up of highly educated white people. The results, therefore, will need to be confirmed on other populations.

A pro-inflammatory factor

“These data seem to support observations already available to the scientific community – comments a Salute Alessandro Padovani, president of the Italian Society of Neurology (Sin) – Air pollution, like other environmental factors, is to be considered a contributory cause of the onset of forms of neurodegeneration, and it has been estimated that it can account for up to 1% in the development of all forms of dementia”. The mechanism by which atmospheric particulates such as PM 2.5 could intervene to the detriment of the health of the nervous system is the same as recognized for the cardio-cerebrovascular system: promoting chronic systemic inflammation. “Everything that fuels a perennial inflammatory state, including other conditions such as diabetes, contributes to increasing the risk of dementia – concludes Padovani – From this perspective, air pollution must also be considered: that is, as a factor, among the others, which can accelerate the production of neuropathological alterations, but which alone is not sufficient to trigger neurodegeneration”.

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