Long-term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid β-42 and α-Synuclein in Children and Young Adults

@article{CaldernGarcidueas2008LongtermAP,
  title={Long-term Air Pollution Exposure Is Associated with Neuroinflammation, an Altered Innate Immune Response, Disruption of the Blood-Brain Barrier, Ultrafine Particulate Deposition, and Accumulation of Amyloid $\beta$-42 and $\alpha$-Synuclein in Children and Young Adults},
  author={Lilian Calder{\'o}n-Garcidue{\~n}as and Anna C Solt and Carlos F. Henr{\'i}quez-Rold{\'a}n and Ricardo Torres‐Jard{\'o}n and Bryan L. Nuse and Lou A. Herritt and Rafael Villarreal-Calder{\'o}n and Norma Osnaya and Ida M. Stone and Raquel Garc{\'i}a and Diane M. Brooks and Ang{\'e}lica G{\'o}nzalez‐Maciel and Rafael Reynoso-Robles and Ricardo Delgado-Ch{\'a}vez and William Reed},
  journal={Toxicologic Pathology},
  year={2008},
  volume={36},
  pages={289 - 310}
}
Air pollution is a serious environmental problem. We investigated whether residency in cities with high air pollution is associated with neuroinflammation/neurodegeneration in healthy children and young adults who died suddenly. We measured mRNA cyclooxygenase-2, interleukin-1β, and CD14 in target brain regions from low (n = 12) or highly exposed residents (n = 35) aged 25.1 ± 1.5 years. Upregulation of cyclooxygenase-2, interleukin-1β, and CD14 in olfactory bulb, frontal cortex, substantia… 

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References

SHOWING 1-10 OF 102 REFERENCES
Brain Inflammation and Alzheimer's-Like Pathology in Individuals Exposed to Severe Air Pollution
TLDR
Exposure to severe airpollution is associated with brain inflammation and Aβ 42 accumulation, two causes of neuronal dysfunction that precede the appearance of neuritic plaques and neurofibrillary tangles, hallmarks of Alzheimer's disease.
DNA Damage in Nasal and Brain Tissues of Canines Exposed to Air Pollutants Is Associated with Evidence of Chronic Brain Inflammation and Neurodegeneration
TLDR
There was an acceleration of Alzheimer's-type pathology in dogs chronically exposed to air pollutants, suggesting that Alzheimer's disease may be the sequela of air pollutant exposures and the resulting systemic inflammation.
Pediatric Respiratory and Systemic Effects of Chronic Air Pollution Exposure: Nose, Lung, Heart, and Brain Pathology
TLDR
The findings of nasal barrier disruption, systemic inflammation, and the upregulation of COX2 and IL-1β expression and Aβ42 accumulation in brain suggests that sustained exposures to significant concentrations of air pollutants such as particulate matter could be a risk factor for AD and other neurodegenerative diseases.
Air Pollution and Brain Damage
TLDR
Persistent pulmonary infl ammation and deteriorating olfactory and respiratory barriers may play a role in the neuropathology observed in the brains of these highly exposed canines.
Innate immune receptor expression in normal brain aging
Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease
  • R. Cutler, J. Kelly, M. Mattson
  • Biology, Chemistry
    Proceedings of the National Academy of Sciences of the United States of America
  • 2004
TLDR
These findings suggest a sequence of events in the pathogenesis of AD in which Aβ induces membrane-associated oxidative stress, resulting in perturbed ceramide and cholesterol metabolism which, in turn, triggers a neurodegenerative cascade that leads to clinical disease.
Differential regulation of the lung endothelin system by urban particulate matter and ozone.
TLDR
The data indicate that ozone and particulate matter independently regulate the expression of lung endothelin system genes, but show complex toxicological interaction with respect to plasma ET-1.
Chronic thrombin exposure results in an increase in apolipoprotein‐E levels
TLDR
It is suggested that thrombin released during brain injury may contribute to an increase in apolipoprotein‐E levels and such increase in Apolipopprotein‐E4 isoform facilitates β‐amyloid deposition and cognitive deficits.
Elevated Plasma Endothelin-1 and Pulmonary Arterial Pressure in Children Exposed to Air Pollution
TLDR
Chronic exposure of children to PM2.5 is associated with increased levels of circulating endothelin-1 and elevated mean pulmonary arterial pressure.
...
...