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@ARTICLE{Rauchmann:165257,
      author       = {Rauchmann, Boris Stephan and Brendel, Matthias and
                      Franzmeier, Nicolai and Trappmann, Lena and Zaganjori,
                      Mirlind and Ersoezlue, Ersin and Morenas-Rodriguez, Estrella
                      and Guersel, Selim and Burow, Lena and Kurz, Carolin and
                      Haeckert, Jan and Tatò, Maia and Utecht, Julia and Papazov,
                      Boris and Pogarell, Oliver and Janowitz, Daniel and Bürger,
                      Katharina and Ewers, Michael and Palleis, Carla and
                      Weidinger, Endy and Biechele, Gloria and Schuster, Sebastian
                      and Finze, Anika and Eckenweber, Florian and Rupprecht,
                      Rainer and Rominger, Axel and Goldhardt, Oliver and Grimmer,
                      Timo and Keeser, Daniel and Stoecklein, Sophia and Dietrich,
                      Olaf and Bartenstein, Peter and Levin, Johannes and
                      Höglinger, Günter and Perneczky, Robert},
      title        = {{M}icroglial {A}ctivation and {C}onnectivity in {A}lzheimer
                      {D}isease and {A}ging.},
      journal      = {Annals of neurology},
      volume       = {92},
      number       = {5},
      issn         = {0364-5134},
      address      = {Hoboken, NJ},
      publisher    = {Wiley-Blackwell},
      reportid     = {DZNE-2022-01550},
      pages        = {768 - 781},
      year         = {2022},
      note         = {CC BY-NC: https://creativecommons.org/licenses/by-nc/4.0/},
      abstract     = {Alzheimer disease (AD) is characterized by amyloid β (Aβ)
                      plaques and neurofibrillary tau tangles, but increasing
                      evidence suggests that neuroinflammation also plays a key
                      role, driven by the activation of microglia. Aβ and tau
                      pathology appear to spread along pathways of highly
                      connected brain regions, but it remains elusive whether
                      microglial activation follows a similar distribution
                      pattern. Here, we assess whether connectivity is associated
                      with microglia activation patterns.We included 32
                      Aβ-positive early AD subjects (18 women, 14 men) and 18
                      Aβ-negative age-matched healthy controls (10 women, 8 men)
                      from the prospective ActiGliA (Activity of Cerebral
                      Networks, Amyloid and Microglia in Aging and Alzheimer's
                      Disease) study. All participants underwent microglial
                      activation positron emission tomography (PET) with the
                      third-generation mitochondrial 18 kDa translocator protein
                      (TSPO) ligand [18 F]GE-180 and magnetic resonance imaging
                      (MRI) to measure resting-state functional and structural
                      connectivity.We found that inter-regional covariance in
                      TSPO-PET and standardized uptake value ratio was
                      preferentially distributed along functionally highly
                      connected brain regions, with MRI structural connectivity
                      showing a weaker association with microglial activation. AD
                      patients showed increased TSPO-PET tracer uptake bilaterally
                      in the anterior medial temporal lobe compared to controls,
                      and higher TSPO-PET uptake was associated with cognitive
                      impairment and dementia severity in a disease
                      stage-dependent manner.Microglial activation distributes
                      preferentially along highly connected brain regions, similar
                      to tau pathology. These findings support the important role
                      of microglia in neurodegeneration, and we speculate that
                      pathology spreads throughout the brain along vulnerable
                      connectivity pathways. ANN NEUROL 2022.},
      keywords     = {Male / Humans / Female / Alzheimer Disease: pathology /
                      Amyloid beta-Peptides: metabolism / Microglia: metabolism /
                      tau Proteins: metabolism / Ligands / Prospective Studies /
                      Positron-Emission Tomography: methods / Plaque, Amyloid:
                      metabolism / Brain: pathology / Receptors, GABA: metabolism
                      / Amyloid beta-Peptides (NLM Chemicals) / tau Proteins (NLM
                      Chemicals) / Ligands (NLM Chemicals) / TSPO protein, human
                      (NLM Chemicals) / Receptors, GABA (NLM Chemicals)},
      cin          = {AG Simons / AG Haass old / Clinical Dementia Research
                      München / AG Höglinger 2},
      ddc          = {610},
      cid          = {I:(DE-2719)1110008 / I:(DE-2719)1110007 /
                      I:(DE-2719)1111016 / I:(DE-2719)1111015},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 351 -
                      Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-351 /
                      G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36053756},
      doi          = {10.1002/ana.26465},
      url          = {https://pub.dzne.de/record/165257},
}