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Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative conditions in older adults, affecting a combined 36 million people worldwide. Evidence suggests that exposure to air pollution increases the risk of developing these diseases. Findings from a recent study demonstrate that particulate matter in air pollution accumulates in the brains of young adults and may serve as a common denominator in the pathophysiology of AD and PD.

Particulate matter in air pollution is a mixture of solid particles and liquid droplets. It is present in fine inhalable particles, with diameters that are generally 2.5 micrograms or less. Ultrafine particles less than 1 microgram in diameter, referred to as nanoparticles, are often enriched in highly reactive metals such as iron, aluminum, titanium, and others. They may serve as catalysts for reactive oxygen species formation and promote protein misfolding and aggregation. Nanoparticles in air pollution are not regulated and carry many health risks. They are also present in food additives and food packaging materials.

The authors of the study documented biomarkers of AD and PD present in brainstem samples taken during the autopsies of 186 healthy children and young adults (age range, 11 months to 27 years) living in the metro area of Mexico City, a region known for its high levels of air pollution. They also conducted magnetic remanence studies to quantify the presence of metal-rich nanoparticles in the brainstem samples. Finally, using high resolution scanning and transmission electron microscopy and energy-dispersive X ray analysis, they identified the composition, location, size, and shape of nanoparticles in the substantia nigra region of a randomly chosen single sample taken from the larger group. Damage to the substantia nigra is a hallmark of PD.

They found that all of the brainstem samples contained iron-, aluminum-, and titanium-rich nanoparticles. The quantity of nanoparticles varied among the brain samples, likely due to the level and duration of exposure. The authors posited that these nanoparticles could have been acquired via both oral and respiratory routes from food sources and airborne exposures, respectively. Damage to the mitochondria, endoplasmic reticulum, and neuromelanin in the single brainstem sample correlated with the presence of iron-, aluminum-, and titanium-rich nanoparticles.

These findings suggest that exposure to nanoparticles is pervasive, with evidence confirmed as early as 11 months of age. Such exposures may put people living in urban areas where high levels of air pollutants are present at greater risk for developing AD and PD.

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