PM2.5, O3 pollution related to Alzheimer's disease development; a new study identifies axonal damage that changes

Exhibitions for PM gatherings2.5 and ozone at or above the current levels has been linked to neuroimflammation and high risk of Alzheimer's disease (AD). The 2015 study found a risk of 138% increase in AD due to an increase of 4.34 μg / m3 in PM2.5 a long-term recommendation to PM2.5, as well as ozone over current EPA levels, is linked to increased risk of Alzheimer's disease.

Now, there is a new study of children and young adults in Mexico City with a team of researchers at Montana Universities, Valle de México, Boise State, Veracruzana University, National Institute of Pediatrics and Paul-Flechsig Institute for Brain Research to identify to promote axonal damage and assay Neo-P-Tau assay for fluid cerebrospinal (CSF) assay.

The study is about raising concerns about Alzheimer's psychology; growing and problematic in the urban cities of the City City (MMC). These results are published in the & # 39; Journal of Alzheimer's DiseaseSouth Westerly

Mexico City Metropolitan (MMC) is an example of urban growth and poor environmental pollution; millions of children are independently exposed to damaging assemblies of PM2.5 every day from the beginning.

This study aimed at investigating a normal 507 CSF of symbols from children, teenagers and young adults aged 12.8 ± 6.7 years from MMC and control of cities with low levels of air pollution, and & # 39; Using unconnected uncontrolled monoclonal (Non-P-Tau) high-tech compression capable of damaging AD and axonal.

In 81 samples, researchers also had a total tau (T-Tau) measure, tph fosphorylated at threonine 181 (P-Tau), amyloid-β 1-42, neurotrophic factor (BDNF), brain, leptin and slaves. A

The authors are recorded with axonal microscopy (TEM) millennium volume, and the associated knowledge of nanoparticles (CDNPs) from falling (CDNP)) CDNPs rich, very seriously in a shorter case (ACC) in 6 young people (4 MMCs, 2 controls).

Non-P-Tau showed a strong rise with a much quicker age among MMC versus controls. A cingulate craft was previously seen in the average axonal size and CDNP related to organelle biology in MMC residents.

Ne-P-Tau revealed a significant increase in age-finding in a young population where changes are currently occurring and HR-designated indicators are constantly changing in the case. first two decades of life. Neo-P-Tau can be an early bio-signal of axonal damage and axonal AD geophysics in totally open young numbers.

The international team of researchers should say that efforts should be aimed at environmental features that may affect Alzheimer's disease development and to reduce the risk of alzheimer's disease. adversely affecting children and young adults to be a public health priority to stop HR development in the first forty of life.


  • Calderón-Garcidueñas et al. (2018) "A Flu in Cerebrospinal Fluid is a Signal of Alzheimer's Disease in the Young Urbanites that was sent to Air Pollution" Journal of Alzheimer's Disease, vol. 66, gun. 4, pp. 1437-1451 doi: 10.3233 / JAD-180853

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