A recent study investigated a potential association between specific amino acids and an elevated risk of dementia associated with exposure to PM2.5 air pollution. Even though the research was inconclusive, it did highlight the need for more research into the mechanisms underlying how air pollution affects the brain by pointing to the possibility that high homocysteine or low methionine levels may combine with pollution to increase dementia risk.
According to a study recently published in Neurology, the official journal of the American Academy of Neurology, amino acids related to vitamin B may be connected to the risk of dementia linked to a particular kind of air pollution known as particulate matter. Although the study does not prove a link between pollution or amino acids and dementia, it does suggest a possible interaction between both.
Fine particulate matter, or P M2.5, is a term used to describe airborne pollutants with a diameter of less than 2.5 microns. Two other amino acids, methionine and homocysteine, were also examined. Methionine, an important amino acid, is involved in typical brain functions and can be found in foods like meat, fish, dairy products, beans, and eggs.
Homocysteine is an amino acid made in the cells that can be converted to methionine through a process that needs both folate, a nutrient crucial for good cell growth and function, and vitamin B12, both vital for creating red blood cells.
According to research author Giulia Grande, MD, PhD, of the Karolinska Institutet in Stockholm, Sweden, “previous studies have found a link between air pollution and dementia risk, but we don’t have a good understanding of the mechanisms through which air pollution impacts the brain.” In this investigation, they discovered that two vitamin B-related amino acid classes were associated with the risk of dementia brought on by air pollution.
Over 2,500 senior citizens in central Stockholm, with an average age of 73, were tracked for up to 12 years for the study. 376 of them eventually developed dementia. Participants completed questionnaires on their eating and exercise routines and had interviews and blood testing.
The researchers then determined the annual average PM2.5 concentrations at the subjects’ residential addresses. The average exposure to PM2.5 pollution for those who got dementia was 8.4 micrograms per cubic meter (g/m3), compared to 8.3 g/m3 for those who did not. These yearly average PM2.5 concentrations are modest compared to the 13.8 g/m3 average for the rest of Europe.
Age, sex, smoking, education, and other factors that may influence a person’s risk of dementia were taken into account, and the researchers discovered that for every one g/m3 increase in PM2.5 exposures over the five years before the study’s commencement, the chance of dementia increased by 70%. The next step was to determine if the amino acids impacted how dementia was altered by exposure to air pollution.
Overall, researchers discovered that an interaction between air pollution and high homocysteine levels or low methionine levels was responsible for nearly half of the increased risk of dementia caused by PM2.5.
The findings suggested that low methionine levels and elevated homocysteine levels contributed to the dementia risk associated with air pollution. Still, they also demonstrated a significant direct effect of air pollution on dementia, indicating that air pollution affects the progression of dementia through several pathways.
This underlines the need for more investigation into the precise biological processes behind the brain damage brought on by air pollution. The study was sponsored by the Swedish Research Council, the Swedish Research Council for Health, Working Life, and Welfare, as well as other Swedish foundations.
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