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001     137449
005     20240321220242.0
024 7 _ |a 10.1523/JNEUROSCI.5002-13.2014
|2 doi
024 7 _ |a pmid:24948809
|2 pmid
024 7 _ |a pmc:PMC6608212
|2 pmc
024 7 _ |a 0270-6474
|2 ISSN
024 7 _ |a 1529-2401
|2 ISSN
024 7 _ |a altmetric:2448613
|2 altmetric
037 _ _ |a DZNE-2020-03771
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Bodea, Liviu-Gabriel
|0 P:(DE-HGF)0
|b 0
245 _ _ |a Neurodegeneration by activation of the microglial complement-phagosome pathway.
260 _ _ |a Washington, DC
|c 2014
|b Soc.57413
264 _ 1 |3 online
|2 Crossref
|b Society for Neuroscience
|c 2014-06-18
264 _ 1 |3 print
|2 Crossref
|b Society for Neuroscience
|c 2014-06-18
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 1585311018_16440
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Systemic inflammatory reactions have been postulated to exacerbate neurodegenerative diseases via microglial activation. We now demonstrate in vivo that repeated systemic challenge of mice over four consecutive days with bacterial LPS maintained an elevated microglial inflammatory phenotype and induced loss of dopaminergic neurons in the substantia nigra. The same total cumulative LPS dose given within a single application did not induce neurodegeneration. Whole-genome transcriptome analysis of the brain demonstrated that repeated systemic LPS application induced an activation pattern involving the classical complement system and its associated phagosome pathway. Loss of dopaminergic neurons induced by repeated systemic LPS application was rescued in complement C3-deficient mice, confirming the involvement of the complement system in neurodegeneration. Our data demonstrate that a phagosomal inflammatory response of microglia is leading to complement-mediated loss of dopaminergic neurons.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
|0 G:(DE-HGF)POF3-342
|c POF3-342
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Complement C3
|2 NLM Chemicals
650 _ 7 |a Complement System Proteins
|0 9007-36-7
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Complement Activation: physiology
|2 MeSH
650 _ 2 |a Complement C3: metabolism
|2 MeSH
650 _ 2 |a Complement System Proteins: physiology
|2 MeSH
650 _ 2 |a Dopaminergic Neurons: metabolism
|2 MeSH
650 _ 2 |a Dopaminergic Neurons: pathology
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, 129 Strain
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Mice, Knockout
|2 MeSH
650 _ 2 |a Microglia: metabolism
|2 MeSH
650 _ 2 |a Microglia: pathology
|2 MeSH
650 _ 2 |a Nerve Degeneration: metabolism
|2 MeSH
650 _ 2 |a Nerve Degeneration: pathology
|2 MeSH
650 _ 2 |a Neural Pathways: physiology
|2 MeSH
650 _ 2 |a Phagosomes: metabolism
|2 MeSH
650 _ 2 |a Phagosomes: pathology
|2 MeSH
650 _ 2 |a Phagosomes: physiology
|2 MeSH
700 1 _ |a Wang, Yiner
|0 P:(DE-HGF)0
|b 1
700 1 _ |a Linnartz-Gerlach, Bettina
|0 P:(DE-HGF)0
|b 2
700 1 _ |a Kopatz, Jens
|0 P:(DE-HGF)0
|b 3
700 1 _ |a Sinkkonen, Lasse
|0 P:(DE-HGF)0
|b 4
700 1 _ |a Musgrove, Ruth
|0 P:(DE-2719)2810507
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|u dzne
700 1 _ |a Kaoma, Tony
|0 P:(DE-HGF)0
|b 6
700 1 _ |a Muller, Arnaud
|0 P:(DE-HGF)0
|b 7
700 1 _ |a Vallar, Laurent
|0 P:(DE-HGF)0
|b 8
700 1 _ |a Di Monte, Donato A
|0 P:(DE-2719)2481741
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700 1 _ |a Balling, Rudi
|0 P:(DE-HGF)0
|b 10
700 1 _ |a Neumann, Harald
|0 P:(DE-HGF)0
|b 11
|e Corresponding author
773 1 8 |a 10.1523/jneurosci.5002-13.2014
|b Society for Neuroscience
|d 2014-06-18
|n 25
|p 8546-8556
|3 journal-article
|2 Crossref
|t Journal of Neuroscience
|v 34
|y 2014
|x 0270-6474
773 _ _ |a 10.1523/JNEUROSCI.5002-13.2014
|g Vol. 34, no. 25, p. 8546 - 8556
|0 PERI:(DE-600)1475274-8
|n 25
|q 34:25<8546 - 8556
|p 8546-8556
|t The journal of neuroscience
|v 34
|y 2014
|x 0270-6474
856 7 _ |2 Pubmed Central
|u http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6608212
909 C O |o oai:pub.dzne.de:137449
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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