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A recent study explored a potential connection between certain amino acids and increased dementia risk linked to PM2.5 air pollution exposure. While not conclusive, the research suggested that high homocysteine or low methionine levels may interact with pollution to elevate dementia risk, emphasizing the need for a deeper understanding of the mechanisms behind air pollution’s impact on the brain.
Elevated levels of amino acids that are related to vitamin B have been found to potentially contribute to the risk of dementia associated with a specific type of air pollutant called particulate matter, according to a recent study published in Neurology, the medical journal of the American Academy of Neurology. While the study does not prove a direct cause-and-effect relationship between pollution or amino acids and dementia, it suggests a possible link between them.
The researchers examined fine particulate matter, PM2.5, which is composed of pollutant particles with a diameter of less than 2.5 microns suspended in the air. They also investigated two amino acids, methionine and homocysteine. Methionine is an essential amino acid found in foods such as meat, fish, dairy, beans, and eggs, and it plays a role in normal brain function. Homocysteine is an amino acid produced by cells and can be converted to methionine through a reaction that requires both vitamin B12 and folate, a nutrient important for red blood cell formation and overall cellular health and function.
“Previous studies have identified a connection between air pollution and the risk of dementia, but the mechanisms through which air pollution affects the brain are not well understood,” said study author Giulia Grande, MD, PhD, from the Karolinska Institutet in Stockholm, Sweden. “In this study, we found that two types of vitamin B-related amino acids played a role in increasing or decreasing the risk of dementia associated with air pollution.”
The study followed over 2,500 adults with an average age of 73 living in central Stockholm for up to 12 years. Out of the participants, 376 individuals developed dementia.
During the study, participants underwent interviews, blood tests, and provided information about their physical activity and diet.
The researchers then calculated the yearly average levels of PM2.5 at the participants’ home addresses. The individuals who developed dementia had an average exposure to PM2.5 pollution of 8.4 micrograms per cubic meter (µg/m3), compared to 8.3 µg/m3 for those who did not develop dementia. These annual average levels of PM2.5 are relatively low compared to the average levels in other parts of Europe, which are 13.8 μg/m3.
After adjusting for various factors that can influence dementia risk, such as age, sex, smoking, and education, the researchers discovered that the risk of dementia increased by 70% for every one µg/m3 increase in PM2.5 exposure during the five years prior to the study.
The researchers also examined whether the impact of air pollution on dementia was influenced by the amino acids.
Overall, the study revealed that approximately half of the increased dementia risk associated with PM2.5 was due to an interaction between air pollution and high homocysteine levels or low methionine levels.
“Our findings suggest that elevated homocysteine levels and low methionine levels contribute to the dementia risk associated with air pollution, but we also observed a significant direct effect of air pollution on dementia, indicating that air pollution impacts the development of dementia through multiple pathways,” said Grande. “This underlines the importance of further research into the precise biological mechanisms underlying the brain damage caused by air pollution.”
Reference: “Association of Long-term Exposure to Air Pollution and Dementia Risk – The Role of Homocysteine, Methionine, and Cardiovascular Burden” by Giulia Grande, Babak Hooshmand, Davide Liborio Vetrano, David A Smith, Helga Refsum, Laura Fratiglioni, Petter Ljungman, Jing Wu, Andrea Bellavia, Kristina Eneroth, Tom Bellander, and Debora Rizzuto, 13 July 2023, Neurology.
DOI: 10.1212/WNL.0000000000207656
A potential limitation of the study is that it only focused on the Kungsholmen district of Stockholm, which is relatively small, limiting comparisons regarding air pollutants.
The study was funded by the Swedish Ministry of Health and Social Affairs, the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, and several Swedish foundations.