Monday , February 6 2023

PM2.5, O3 pollution due to Alzheimer's disease development; The new job identifies the change of axonal damage



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PM concentrations2.5 and existing standards or above-mentioned ozones are associated with high risk of neuroinflammation and Alzheimer's disease. In the 2015 study, the risk of AD increased by 4.34 micrograms / m3 At PM2.5 He has long been exposed to the PM2.5, as well as the existing US EPA standards, are associated with increased risk of Alzheimer's disease.

Nowadays, a non-P-Tau test for advanced cerebrospinal fluid in children and adolescents in Mexico, by a team of researchers at Montana State Universities, Valle de Mexiko, Boise Province, Universidad Veracruzana, Instituto Nacional de Pediatrics and Paul-Fertility-Brain Research Institute CSF) axonal damage.

The research creates anxiety over the developmental and relentless Alzheimer's pathology observed in young Metropolitan Mexico City (MMC) urbanites. These findings are published Journal of Alzheimer's Disease.

Metropolitan Mexico City (MMC) is an example of extreme urban growth and serious environmental pollution; millions of children are exposed to harmful concentrations of any PM2.5 Every day since the concept.

This study revealed that 507 CSF normal samples of children, adolescents and adolescents with moderate levels of air pollutants from the MMC and control cities were 12.8 ± 6.7 years with high affinity monoclonal non-phosphorylated tau antibody (Non-P-Tau) AD and potential biomarker for aconal damage .

In 81 specimens, researchers measured tau (T-Tau) phosphorylate in total tau (T-Tau), threonine 181 (P-Tau), amyloid-β 1-42, cerebral neurotrophic factor (BDNF), insulin, leptin and inflammatory mediators . A

Transaminated electron microscopy (TEM) with myelinated axonal size and combustion with nanoparticle (CDNP) authors – High oxidant CDNP – 2 controls in anterior cingulate cortex (ACC) with 6 young calendars (4 MMCs).

The relationship between Non-P-Tau LLC and the mutual control showed a relatively stronger age. Anterior syndrome cortex showed a significant reduction in the mean flow size and showed that CDNP & apos; s are associated with organelle pathology in MMC residents.

Non-P-Tau is an important finding in the young population experiencing fluctuations in the age of significant increases in age and AD rings develop in a constant way in the first two decades of life. Non-P-Tau is potentially an early biomarker and AD axonal pathology of Axonal damage in exposed young people.

A group of international researchers should focus on identifying and reducing environmental impacts that affect the development of Alzheimer's disease, and nervous protection of children and adolescents should be a priority for public health to stop AD development in the first 20 years of life.

Resources

  • Calderón-Garcidueñas and so on. (2018) "Non-Phosphorylated Tau in the Cerebrospinal Fluid, Continuum Marker of Alzheimer's Disease in Young Urbanites Affected by Air Pollution" Journal of Alzheimer's Diseaseskin 66, no. 4, p. 1437-1451 doi: 10.3233 / JAD-180853

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