Home > Publications Database > Benzo(a)pyrene exposure induced neuronal loss, plaque deposition, and cognitive decline in APP/PS1 mice > print

001     153452
005     20240420115851.0
024 7 _ |a pmc:PMC7461337
|2 pmc
024 7 _ |a 10.1186/s12974-020-01925-y
|2 doi
024 7 _ |a altmetric:89245490
|2 altmetric
024 7 _ |a pmid:32867800
|2 pmid
037 _ _ |a DZNE-2020-01449
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Liu, Dan
|0 P:(DE-2719)2813521
|b 0
|e First author
245 _ _ |a Benzo(a)pyrene exposure induced neuronal loss, plaque deposition, and cognitive decline in APP/PS1 mice
260 _ _ |a London
|c 2020
|b BioMed Central
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1713529057_11036
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a BackgroundExposure 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.
536 _ _ |a 345 - Population Studies and Genetics (POF3-345)
|0 G:(DE-HGF)POF3-345
|c POF3-345
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Amyloid beta-Protein Precursor: genetics
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Behavior, Animal: drug effects
|2 MeSH
650 _ 2 |a Benzo(a)pyrene: toxicity
|2 MeSH
650 _ 2 |a Cognitive Dysfunction: chemically induced
|2 MeSH
650 _ 2 |a Cognitive Dysfunction: pathology
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Exploratory Behavior: drug effects
|2 MeSH
650 _ 2 |a Maze Learning: drug effects
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Neurons: drug effects
|2 MeSH
650 _ 2 |a Neurons: pathology
|2 MeSH
650 _ 2 |a Plaque, Amyloid: pathology
|2 MeSH
650 _ 2 |a Presenilin-1: genetics
|2 MeSH
650 _ 2 |a Spatial Memory: drug effects
|2 MeSH
700 1 _ |a Zhao, Yujia
|b 1
700 1 _ |a Qi, Yuze
|b 2
700 1 _ |a Gao, Yun
|b 3
700 1 _ |a Tu, Dezhen
|b 4
700 1 _ |a Wang, Yinxi
|b 5
700 1 _ |a Gao, Hui-Ming
|0 P:(DE-HGF)0
|b 6
|e Corresponding author
700 1 _ |a Zhou, Qihui
|0 P:(DE-HGF)0
|b 7
|e Corresponding author
773 _ _ |a 10.1186/s12974-020-01925-y
|g Vol. 17, no. 1, p. 258
|0 PERI:(DE-600)2156455-3
|n 1
|p 258
|t Journal of neuroinflammation
|v 17
|y 2020
|x 1742-2094
856 4 _ |u https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-020-01925-y
856 4 _ |u https://pub.dzne.de/record/153452/files/DZNE-2020-01449.pdf
|y OpenAccess
856 4 _ |u https://pub.dzne.de/record/153452/files/DZNE-2020-01449.pdf?subformat=pdfa
|x pdfa
|y OpenAccess
909 C O |o oai:pub.dzne.de:153452
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 0
|6 P:(DE-2719)2813521
913 1 _ |a DE-HGF
|b Gesundheit
|l Erkrankungen des Nervensystems
|1 G:(DE-HGF)POF3-340
|0 G:(DE-HGF)POF3-345
|3 G:(DE-HGF)POF3
|2 G:(DE-HGF)POF3-300
|4 G:(DE-HGF)POF
|v Population Studies and Genetics
|x 0
913 2 _ |a DE-HGF
|b Programmungebundene Forschung
|l ohne Programm
|1 G:(DE-HGF)POF4-890
|0 G:(DE-HGF)POF4-899
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-800
|4 G:(DE-HGF)POF
|v ohne Topic
|x 0
914 1 _ |y 2020
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2023-03-30
915 _ _ |a Creative Commons Attribution CC BY (No Version)
|0 LIC:(DE-HGF)CCBYNV
|2 V:(DE-HGF)
|b DOAJ
|d 2020-09-04
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2023-03-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2020-09-04
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
|d 2023-03-30
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b J NEUROINFLAMM : 2021
|d 2023-03-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
|d 2023-03-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
|d 2022-08-15T08:22:49Z
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2020-09-04
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
|d 2022-08-15T08:22:49Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2023-03-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2023-03-30
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
|d 2023-03-30
915 _ _ |a Article Processing Charges
|0 StatID:(DE-HGF)0561
|2 StatID
|d 2020-09-04
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b J NEUROINFLAMM : 2021
|d 2023-03-30
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2020-09-04
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2023-03-30
915 _ _ |a Fees
|0 StatID:(DE-HGF)0700
|2 StatID
|d 2020-09-04
920 1 _ |0 I:(DE-2719)1012001
|k AG Breteler
|l Population Health Sciences
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-2719)1012001
980 1 _ |a FullTexts

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21