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000153452 041__ $$aEnglish
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000153452 1001_ $$0P:(DE-2719)2813521$$aLiu, Dan$$b0$$eFirst author
000153452 245__ $$aBenzo(a)pyrene exposure induced neuronal loss, plaque deposition, and cognitive decline in APP/PS1 mice
000153452 260__ $$aLondon$$bBioMed Central$$c2020
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000153452 520__ $$aBackgroundExposure to benzo(a)pyrene (BaP) was associated with cognitive impairments and some Alzheimer’s disease (AD)-like pathological changes. However, it is largely unknown whether BaP exposure participates in the disease progression of AD.ObjectivesTo investigate the effect of BaP exposure on AD progression and its underlying mechanisms.MethodsBaP or vehicle was administered to 4-month-old APPswe/PS1dE9 transgenic (APP/PS1) mice and wildtype (WT) mice for 2 months. Learning and memory ability and exploratory behaviors were evaluated 1 month after the initiation/termination of BaP exposure. AD-like pathological and biochemical alterations were examined 1 month after 2-month BaP exposure. Levels of soluble beta-amyloid (Aβ) oligomers and the number of Aβ plaques in the cortex and the hippocampus were quantified. Gene expression profiling was used to evaluate alternation of genes/pathways associated with AD onset and progression. Immunohistochemistry and Western blot were used to demonstrate neuronal loss and neuroinflammation in the cortex and the hippocampus. Treatment of primary neuron-glia cultures with aged Aβ (a mixture of monomers, oligomers, and fibrils) and/or BaP was used to investigate mechanisms by which BaP enhanced Aβ-induced neurodegeneration.ResultsBaP exposure induced progressive decline in spatial learning/memory and exploratory behaviors in APP/PS1 mice and WT mice, and APP/PS1 mice showed severer behavioral deficits than WT mice. Moreover, BaP exposure promoted neuronal loss, Aβ burden and Aβ plaque formation in APP/PS1 mice, but not in WT mice. Gene expression profiling showed most robust alteration in genes and pathways related to inflammation and immunoregulatory process, Aβ secretion and degradation, and synaptic formation in WT and APP/PS1 mice after BaP exposure. Consistently, the cortex and the hippocampus of WT and APP/PS1 mice displayed activation of microglia and astroglia and upregulation of inducible nitric oxide synthase (iNOS), glial fibrillary acidic protein (GFAP), and NADPH oxidase (three widely used neuroinflammatory markers) after BaP exposure. Furthermore, BaP exposure aggravated neurodegeneration induced by aged Aβ peptide in primary neuron-glia cultures through enhancing NADPH oxidase-derived oxidative stress.ConclusionOur study showed that chronic exposure to environmental pollutant BaP induced, accelerated, and exacerbated the progression of AD, in which elevated neuroinflammation and NADPH oxidase-derived oxidative insults were key pathogenic events.
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000153452 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000153452 650_2 $$2MeSH$$aAmyloid beta-Protein Precursor: genetics
000153452 650_2 $$2MeSH$$aAnimals
000153452 650_2 $$2MeSH$$aBehavior, Animal: drug effects
000153452 650_2 $$2MeSH$$aBenzo(a)pyrene: toxicity
000153452 650_2 $$2MeSH$$aCognitive Dysfunction: chemically induced
000153452 650_2 $$2MeSH$$aCognitive Dysfunction: pathology
000153452 650_2 $$2MeSH$$aDisease Models, Animal
000153452 650_2 $$2MeSH$$aExploratory Behavior: drug effects
000153452 650_2 $$2MeSH$$aMaze Learning: drug effects
000153452 650_2 $$2MeSH$$aMice
000153452 650_2 $$2MeSH$$aNeurons: drug effects
000153452 650_2 $$2MeSH$$aNeurons: pathology
000153452 650_2 $$2MeSH$$aPlaque, Amyloid: pathology
000153452 650_2 $$2MeSH$$aPresenilin-1: genetics
000153452 650_2 $$2MeSH$$aSpatial Memory: drug effects
000153452 7001_ $$aZhao, Yujia$$b1
000153452 7001_ $$aQi, Yuze$$b2
000153452 7001_ $$aGao, Yun$$b3
000153452 7001_ $$aTu, Dezhen$$b4
000153452 7001_ $$aWang, Yinxi$$b5
000153452 7001_ $$0P:(DE-HGF)0$$aGao, Hui-Ming$$b6$$eCorresponding author
000153452 7001_ $$0P:(DE-HGF)0$$aZhou, Qihui$$b7$$eCorresponding author
000153452 773__ $$0PERI:(DE-600)2156455-3$$a10.1186/s12974-020-01925-y$$gVol. 17, no. 1, p. 258$$n1$$p258$$tJournal of neuroinflammation$$v17$$x1742-2094$$y2020
000153452 8564_ $$uhttps://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-020-01925-y
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