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@ARTICLE{Bodea:137449,
      author       = {Bodea, Liviu-Gabriel and Wang, Yiner and Linnartz-Gerlach,
                      Bettina and Kopatz, Jens and Sinkkonen, Lasse and Musgrove,
                      Ruth and Kaoma, Tony and Muller, Arnaud and Vallar, Laurent
                      and Di Monte, Donato A and Balling, Rudi and Neumann,
                      Harald},
      title        = {{N}eurodegeneration by activation of the microglial
                      complement-phagosome pathway.},
      journal      = {The journal of neuroscience},
      volume       = {34},
      number       = {25},
      issn         = {0270-6474},
      address      = {Washington, DC},
      publisher    = {Soc.57413},
      reportid     = {DZNE-2020-03771},
      pages        = {8546-8556},
      year         = {2014},
      abstract     = {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.},
      keywords     = {Animals / Complement Activation: physiology / Complement
                      C3: metabolism / Complement System Proteins: physiology /
                      Dopaminergic Neurons: metabolism / Dopaminergic Neurons:
                      pathology / Male / Mice / Mice, 129 Strain / Mice, Inbred
                      C57BL / Mice, Knockout / Microglia: metabolism / Microglia:
                      pathology / Nerve Degeneration: metabolism / Nerve
                      Degeneration: pathology / Neural Pathways: physiology /
                      Phagosomes: metabolism / Phagosomes: pathology / Phagosomes:
                      physiology / Complement C3 (NLM Chemicals) / Complement
                      System Proteins (NLM Chemicals)},
      cin          = {AG Di Monte},
      ddc          = {610},
      cid          = {I:(DE-2719)1013008},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24948809},
      pmc          = {pmc:PMC6608212},
      doi          = {10.1523/JNEUROSCI.5002-13.2014},
      url          = {https://pub.dzne.de/record/137449},
}