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@INPROCEEDINGS{Schlachetzki:283066,
      author       = {Schlachetzki, Johannes C M and Zhou, Yi and Spann, Nathan
                      and Kleemann, Kilian Leon and McManus, Roisin M and Heneka,
                      Michael T and Butovsky, Oleg and Glass, Christopher K},
      title        = {{D}ecoding transcriptional regulation of microglia
                      associated with amyloid plaques},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {Suppl 1},
      issn         = {1552-5260},
      reportid     = {DZNE-2025-01473},
      pages        = {e106751},
      year         = {2025},
      abstract     = {Beyond the progressive accumulation of amyloid-beta and
                      hyperphosphorylated tau, Alzheimer's disease (AD) is
                      accompanied by phenotypic changes in microglia, the innate
                      immune cells of the brain. In particular, microglia in the
                      vicinity of Amyloid-plaques, also known as MGnD or DAM, are
                      defined by distinct changes in their gene expression
                      signature, e.g., upregulation of Trem2 mRNA. However, the
                      precise transcriptional mechanism that drives microglia
                      phenotype in response to amyloid is not defined.Here, we
                      isolated microglia from the APP/PS1 transgenic mouse model
                      followed by ATAC-seq.We provide evidence for a model in
                      which differential activation of a common set of
                      transcriptional regulators that includes members of the
                      MITF/TFE, AP-1 and EGR transcription factor families drives
                      the amyloid-plaque associated microglia
                      phenotype.Collectively, these findings reveal the framework
                      of the transcriptional circuitry that is used to establish a
                      range of neurodegenerative pathology-associated microglia
                      phenotypes.},
      month         = {Jul},
      date          = {2025-07-27},
      organization  = {Alzheimer’s Association
                       International Conference, Toronto
                       (Canada), 27 Jul 2025 - 31 Jul 2025},
      keywords     = {Animals / Microglia: metabolism / Microglia: pathology /
                      Mice, Transgenic / Alzheimer Disease: pathology / Alzheimer
                      Disease: genetics / Alzheimer Disease: metabolism / Mice /
                      Disease Models, Animal / Plaque, Amyloid: pathology /
                      Plaque, Amyloid: metabolism / Brain: pathology / Brain:
                      metabolism / Amyloid beta-Protein Precursor: genetics /
                      Humans / Amyloid beta-Peptides: metabolism / Presenilin-1:
                      genetics / Amyloid beta-Protein Precursor (NLM Chemicals) /
                      Amyloid beta-Peptides (NLM Chemicals) / Presenilin-1 (NLM
                      Chemicals)},
      cin          = {AG McManus},
      ddc          = {610},
      cid          = {I:(DE-2719)1013042},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
      pubmed       = {pmid:41447077},
      pmc          = {pmc:PMC12739734},
      doi          = {10.1002/alz70855_106751},
      url          = {https://pub.dzne.de/record/283066},
}