Sunday , October 17 2021

PM2.5, O3 pollution associated with the development of Alzheimer's disease; new study identifies axonal damage in evolution

Exposure to PM concentrations2.5 and ozone at or above current standards have been associated with neuroinflammation and high risk of Alzheimer's disease (AD). A 2015 study found a risk of 138% increase in AD by an increase of 4.34 μg / m3 in PM2.5 suggesting prolonged exposure to PM2.5, as well as ozone above current US EPA standards, are associated with increased risk of Alzheimer's disease.

Now a new study of children and young adults in Mexico City by a team of researchers from the Universities of Montana, Valle de México, Boise, Veracruzana University, National Institute of Pediatrics and Paul-Flechsig-Institute for Brain Research identified evolution injury axonal analysis using a new Non-P-Tau cerebrospinal fluid (CSF) assay.

The study raises concerns about the evolution and relentless Alzheimer's pathology observed in urban young people from the Metropolitan City of Mexico (MMC). These findings are published in the Journal of Alzheimer's disease.

The Metropolitan City of Mexico (MMC) is an example of extreme urban growth and severe environmental pollution; millions of children are involuntarily exposed to harmful concentrations of PM2.5 every day since conception.

This study focused on studying 507 normal CSF samples from children, adolescents, and young adults with a mean age of 12.8 ± 6.7 years from MMC and control cities with low levels of air pollutants using a non-phosphorylated monoclonal antibody of tau (Non-P-Tau) as a potential AD marker and axonal damage.

In 81 samples, the researchers also measured total tau (T-Tau), phosphorylated tau in threonine 181 (P-Tau), amyloid-β 1-42, brain derived neurotrophic factor (BDNF), insulin, leptin and inflammatory mediators. AN

The authors documented myelinized axonal size and the pathology associated with combustion-derived nanoparticles (CDNPs) – highly oxidizing, highly oxidant CDNPs in the white matter of the anterior cingulate cortex (ACC) in 6 young residents (4 MMC). , 2 controls).

Non-P-Tau showed a strong increase with significantly faster age between MMC versus controls. The anterior cingulate cortex showed a significant reduction in mean axonal size and CDNPs were associated with organelle pathology in MMC residents.

Non-P-Tau exhibited significant increases with age – an important finding in a young population where axonal changes are present and AD marks are constantly evolving in the first two decades of life. Non-P-Tau is potentially an early biomarker of axonal damage and axonal pathology of AD in highly exposed young populations.

The international team of researchers said efforts should be designed to identify and mitigate the environmental factors that influence the development of Alzheimer's disease and the neuroprotection of children and young adults should be a public health priority to stop the development of AD in the first two decades of life.


  • Calderón-Garcidueñas et al. (2018) "Unphosphorylated tau in cerebrospinal fluid is a marker of the continuum of Alzheimer's disease in urban youth exposed to air pollution" Journal of Alzheimer's diseasevol. 66, no. 4, pp. 1437-1451 doi: 10.3233 / JAD-180853

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