[ad_1]
Alzheimer’s disease, the most common form of dementia, affects about 57 million people all over the world. Now, new research confirms that air pollution Not only is it a known risk factor for multiple chronic diseases, but it could also directly influence the development of this neurodegenerative pathology.
The study, led by scientists from Emory University (USA) and published in the scientific journal PLOS Medicineanalyzed more than 27.8 million Medicare beneficiaries over the age of 65 for almost two decades, between 2000 and 2018.
When the air we breathe influences the brain
The researchers examined the relationship between exposure to fine particle pollution and the onset of Alzheimer’staking into account the presence of chronic diseases such as hypertension, depression and history of cerebrovascular accident (stroke).
The results showed that people exposed to higher levels of pollution had a significantly higher risk of developing Alzheimer’s. Although pathologies such as hypertension and depression barely modified this association, the impact was slightly greater in those who had previously suffered a stroke.

According to the authors, the data suggest that air pollution primarily contributes to the development of Alzheimer’s. through direct mechanisms in the brainrather than through intermediate chronic diseases.
Greater vulnerability after a stroke
The study also highlights that people with a history of stroke could be especially vulnerable to the harmful effects of air pollution on brain health. This interaction between environmental and vascular factors underlines the need to reinforce policies to improve air quality.
“In this large national study in older adults, we observed that long-term exposure to fine particles is associated with an increased risk of Alzheimer’s disease, largely through direct effects on the brain,” the researchers note.
Experts conclude that reducing environmental pollution could become an key strategy to prevent dementia and protect cognitive health of the aging population.
[ad_2]
Source link