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Brain Inflammation and Alzheimer's-Like Pathology in Individuals Exposed to Severe Air Pollution

568

Citations

31

References

2004

Year

TLDR

Air pollution, a complex mix of gases, particles, and organics, has been linked to chronic inflammation and accelerated Alzheimer‑like pathology in dogs, indicating potential adverse effects on the human brain. The study examined whether living in highly polluted cities is associated with brain inflammation in humans. Autopsy brains from lifelong residents of low‑ and high‑pollution cities were analyzed for COX2 expression, Aβ42 accumulation, DNA damage, NF‑κB activation, and APOE genotype. Residents of high‑pollution cities showed markedly increased COX2 expression and Aβ42 accumulation in frontal cortex, hippocampus, and olfactory bulb, indicating that severe air pollution is linked to brain inflammation and early Alzheimer‑like changes.

Abstract

Air pollution is a complex mixture of gases (e.g., ozone), particulate matter, and organic compounds present in outdoor and indoor air. Dogs exposed to severe air pollution exhibit chronic inflammation and acceleration of Alzheimer's-like pathology, suggesting that the brain is adversely affected by pollutants. We investigated whether residency in cities with high levels of air pollution is associated with human brain inflammation. Expression of cyclooxygenase-2 (COX2), an inflammatory mediator, and accumulation of the 42-amino acid form of β-amyloid (A β42), a cause of neuronal dysfunction, were measured in autopsy brain tissues of cognitively and neurologically intact lifelong residents of cities having low (n:9) or high (n:10) levels of air pollution. Genomic DNA apurinic/apyrimidinic sites, nuclear factor- κB activation and apolipoprotein E genotype were also evaluated. Residents of cities with severe air pollution had significantly higher COX2 expression in frontal cortex and hippocampus and greater neuronal and astrocytic accumulation of A β42 compared to residents in low air pollution cities. Increased COX2 expression and A β42 accumulation were also observed in the olfactory bulb. These findings suggest that exposure to severe airpollution is associated with brain inflammation and A β 42 accumulation, two causes of neuronal dysfunction that precede the appearance of neuritic plaques and neurofibrillary tangles, hallmarks of Alzheimer's disease.

References

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