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@ARTICLE{Cangalaya:257592,
      author       = {Cangalaya, Carla and Wegmann, Susanne and Sun, Weilun and
                      Diez, Lisa and Gottfried, Anna and Richter, Karin and
                      Stoyanov, Stoyan and Pakan, Janelle and Fischer,
                      Klaus-Dieter and Dityatev, Alexander},
      title        = {{R}eal-time mechanisms of exacerbated synaptic remodeling
                      by microglia in acute models of systemic inflammation and
                      tauopathy.},
      journal      = {Brain, behavior and immunity},
      volume       = {110},
      issn         = {0889-1591},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {DZNE-2023-00468},
      pages        = {245 - 259},
      year         = {2023},
      abstract     = {Remodeling of synapses by microglia is essential for
                      synaptic plasticity in the brain. However, during
                      neuroinflammation and neurodegenerative diseases, microglia
                      can induce excessive synaptic loss, although the precise
                      underlying mechanisms are unknown. To directly observe
                      microglia-synapse interactions under inflammatory
                      conditions, we performed in vivo two-photon time-lapse
                      imaging of microglia-synapse interactions after bacterial
                      lipopolysaccharide administration to model systemic
                      inflammation, or after inoculation of Alzheimer's disease
                      (AD) brain extracts to model disease-associated
                      neuroinflammatory microglial response. Both treatments
                      prolonged microglia-neuron contacts, decreased basal
                      surveillance of synapses and promoted synaptic remodeling in
                      response to synaptic stress induced by focal single-synapse
                      photodamage. Spine elimination correlated with the
                      expression of microglial complement system/phagocytic
                      proteins and the occurrence of synaptic filopodia. Microglia
                      were observed contacting spines, then stretching and
                      phagocytosing spine head filopodia. Thus, in response to
                      inflammatory stimuli microglia exacerbated spine remodeling
                      through prolonged microglial contact and elimination of
                      spines 'tagged' by synaptic filopodia.},
      keywords     = {Humans / Microglia: metabolism / Tauopathies: metabolism /
                      Alzheimer Disease: metabolism / Synapses: metabolism /
                      Inflammation: metabolism / Alzheimer's disease (Other) / C1q
                      (Other) / C3 (Other) / C3R (Other) / CD68 (Other) /
                      Microglia (Other) / Spine elimination (Other) / Spine head
                      filopodia (Other) / Spine turnover (Other) / Synapse (Other)
                      / Synaptic remodeling (Other) / tau (Other)},
      cin          = {AG Dityatev / AG Wegmann},
      ddc          = {150},
      cid          = {I:(DE-2719)1310007 / I:(DE-2719)1810006},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36906076},
      doi          = {10.1016/j.bbi.2023.02.023},
      url          = {https://pub.dzne.de/record/257592},
}