期刊
TOXICOLOGIC PATHOLOGY
卷 36, 期 2, 页码 289-310出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0192623307313011
关键词
alpha-synuclein; Alzheimer's disease; air pollution; amyloid beta 42; neuroinflammation; Parkinson's disease; ultrafine particulate matter
资金
- NCRR NIH HHS [5 P20 RR015583] Funding Source: Medline
- NIEHS NIH HHS [1R21-ES013293-01] Funding Source: Medline
- NINDS NIH HHS [1KO1 NS046410-01A1] Funding Source: Medline
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-1 beta, 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-1 beta, and CD14 in olfactory bulb, frontal cortex, substantia nigrae and vagus nerves; disruption of the blood-brain barrier; endothelial activation, oxidative stress, and inflammatory cell trafficking were seen in highly exposed subjects. Amyloid beta 42 (A beta 42) immunoreactivity was observed in 58.8% of apolipoprotein E (APOE) 3/3 < 25 y, and 100% of the APOE 4 subjects, whereas alpha-synuclein was seen in 23.5% of < 25 y subjects. Particulate material (PM) was seen in olfactory bulb neurons, and PM < 100 nm were observed in intraluminal erythrocytes from lung, frontal, and trigeminal ganglia capillaries. Exposure to air pollution causes neuroinflammation, an altered brain innate immune response, and accumulation of A beta 42 and alpha-synuclein starting in childhood. Exposure to air pollution should be considered a risk factor for Alzheimer's and Parkinson's diseases, and carriers of the APOE 4 allele could have a higher risk of developing Alzheimer's disease if they reside in a polluted environment.
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