% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@INPROCEEDINGS{Chamoun:145342,
      author       = {Chamoun, Miriam and Nebeling, Felix and Schneider, J and
                      Steffen, Julia and Gu, Ligang and Fuhrmann, Martin},
      title        = {{M}icroglia synapse interaction precedes synapse
                      elimination in mouse models of {AD}},
      journal      = {Glia},
      volume       = {65},
      number       = {S1},
      issn         = {0894-1491},
      reportid     = {DZNE-2020-00698},
      pages        = {E290},
      year         = {2017},
      abstract     = {Microglia are actively surveying the brain parenchyma by
                      protracting and retracting their fine processes. They
                      physically interact with neurons and their synapses and have
                      been shown to influence the morphology of dendritic spines
                      dependent on the contact rate under normal physiological
                      conditions. Under neurodegenerative disease conditions like
                      Alzheimer¶s disease (AD), microglia mediate early synapse
                      loss via the complement system or neuron loss dependent on
                      the fractalkine receptor (CX3CR1). It remains unresolved
                      whether microglia contribute to synapse loss during late
                      disease stages, whether that changes contact rates or
                      involves neuron microglia communication via the CX3CR1
                      receptor. To address these open questions, we carried out
                      time-lapse two-photon in vivo imaging in the hippocampus and
                      cortex of two different mouse models of AD, the APP/PS1 and
                      the 3xTg-AD model. We analyzed dendritic spine loss in
                      relation to microglia contact rates of dendritic spines and
                      with respect to CX3CR1-deficiency under advanced AD-like
                      conditions. We found increased turnover and loss of
                      dendritic spines under AD-like conditions. Furthermore,
                      spine loss in proximity to Aȕ-plaques was ameliorated in
                      CX3CR1-deficient APP/PS1 mice. Surprisingly, the microglia
                      contact rates of dendritic spines before elimination were
                      significantly reduced dependent on CX3CR1-deficiency.
                      Reduced microglia contact rates dependent on
                      CX3CR1-deficiency were consistently found in APP/PS1 and
                      3xTg-AD mice similarly in the cortex and hippocampus. These
                      data indicate that microglia mediate synapse loss via
                      elevated physical synapse interactions dependent on the
                      CX3CR1 receptor under advanced AD-like conditions.},
      month         = {Jul},
      date          = {2017-07-08},
      organization  = {GLIA Edinburgh 2017, Edinburgh
                       (Scotland), 8 Jul 2017 - 11 Jul 2017},
      cin          = {AG Fuhrmann / AG Müller},
      ddc          = {610},
      cid          = {I:(DE-2719)1011004 / I:(DE-2719)1310003},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 344
                      - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
      url          = {https://pub.dzne.de/record/145342},
}