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@ARTICLE{Reichenbach:140482,
      author       = {Reichenbach, Nicole and Delekate, Andrea and Plescher,
                      Monika and Schmitt, Franziska and Krauß, Sybille and Blank,
                      Nelli and Halle, Annett and Petzold, Gabor C},
      title        = {{I}nhibition of {S}tat3-mediated astrogliosis ameliorates
                      pathology in an {A}lzheimer's disease model.},
      journal      = {EMBO molecular medicine},
      volume       = {11},
      number       = {2},
      issn         = {1757-4676},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DZNE-2020-06804},
      pages        = {e9665},
      year         = {2019},
      abstract     = {Reactive astrogliosis is a hallmark of Alzheimer's disease
                      (AD), but its role for disease initiation and progression
                      has remained incompletely understood. We here show that the
                      transcription factor Stat3 (signal transducer and activator
                      of transcription 3), a canonical inducer of astrogliosis, is
                      activated in an AD mouse model and human AD Therefore, using
                      a conditional knockout approach, we deleted Stat3
                      specifically in astrocytes in the APP/PS1 model of AD We
                      found that Stat3-deficient APP/PS1 mice show decreased
                      β-amyloid levels and plaque burden. Plaque-close microglia
                      displayed a more complex morphology, internalized more
                      β-amyloid, and upregulated amyloid clearance pathways in
                      Stat3-deficient mice. Moreover, astrocyte-specific
                      Stat3-deficient APP/PS1 mice showed decreased
                      pro-inflammatory cytokine activation and lower dystrophic
                      neurite burden, and were largely protected from cerebral
                      network imbalance. Finally, Stat3 deletion in astrocytes
                      also strongly ameliorated spatial learning and memory
                      decline in APP/PS1 mice. Importantly, these protective
                      effects on network dysfunction and cognition were
                      recapitulated in APP/PS1 mice systemically treated with a
                      preclinical Stat3 inhibitor drug. In summary, our data
                      implicate Stat3-mediated astrogliosis as an important
                      therapeutic target in AD.},
      keywords     = {Alzheimer Disease: pathology / Animals / Astrocytes:
                      pathology / Cell Proliferation / Disease Models, Animal /
                      Gene Knockout Techniques / Humans / Mice / Mice, Knockout /
                      STAT3 Transcription Factor: analysis / STAT3 Transcription
                      Factor: deficiency / STAT3 Transcription Factor (NLM
                      Chemicals) / STAT3 protein, human (NLM Chemicals) / Stat3
                      protein, mouse (NLM Chemicals)},
      cin          = {AG Petzold ; AG Petzold / AG Bano / AG Krauß / AG Halle},
      ddc          = {610},
      cid          = {I:(DE-2719)1013020 / I:(DE-2719)1013003 /
                      I:(DE-2719)1011006 / I:(DE-2719)1013034},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342) / 344 - Clinical and
                      Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342 /
                      G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30617153},
      pmc          = {pmc:PMC6365929},
      doi          = {10.15252/emmm.201809665},
      url          = {https://pub.dzne.de/record/140482},
}