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@ARTICLE{Xiang:904376,
      author       = {Xiang, Xianyuan and Wind, Karin and Wiedemann, Thomas and
                      Blume, Tanja and Shi, Yuan and Briel, Nils and Beyer, Leonie
                      and Biechele, Gloria and Eckenweber, Florian and Zatcepin,
                      Artem and Lammich, Sven and Ribicic, Sara and Tahirovic,
                      Sabina and Willem, Michael and Deussing, Maximilian and
                      Palleis, Carla and Rauchmann, Boris-Stephan and Gildehaus,
                      Franz-Josef and Lindner, Simon and Spitz, Charlotte and
                      Franzmeier, Nicolai and Baumann, Karlheinz and Rominger,
                      Axel and Bartenstein, Peter and Ziegler, Sibylle and
                      Drzezga, Alexander and Respondek, Gesine and Buerger,
                      Katharina and Perneczky, Robert and Levin, Johannes and
                      Höglinger, Günter U. and Herms, Jochen and Haass,
                      Christian and Brendel, Matthias},
      title        = {{M}icroglial activation states drive glucose uptake and
                      {FDG}-{PET} alterations in neurodegenerative diseases},
      journal      = {Science translational medicine},
      volume       = {13},
      number       = {615},
      issn         = {1946-6234},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {FZJ-2021-05946},
      pages        = {eabe5640},
      year         = {2021},
      abstract     = {2-Deoxy-2-[18F]fluoro-d-glucose positron emission
                      tomography (FDG-PET) is widely used to study cerebral
                      glucose metabolism. Here, we investigated whether the
                      FDG-PET signal is directly influenced by microglial glucose
                      uptake in mouse models and patients with neurodegenerative
                      diseases. Using a recently developed approach for cell
                      sorting after FDG injection, we found that, at cellular
                      resolution, microglia displayed higher glucose uptake than
                      neurons and astrocytes. Alterations in microglial glucose
                      uptake were responsible for both the FDG-PET signal decrease
                      in Trem2-deficient mice and the FDG-PET signal increase in
                      mouse models for amyloidosis. Thus, opposite microglial
                      activation states determine the differential FDG uptake.
                      Consistently, 12 patients with Alzheimer’s disease and 21
                      patients with four-repeat tauopathies also exhibited a
                      positive association between glucose uptake and microglial
                      activity as determined by 18F-GE-180 18-kDa translocator
                      protein PET (TSPO-PET) in preserved brain regions,
                      indicating that the cerebral glucose uptake in humans is
                      also strongly influenced by microglial activity. Our
                      findings suggest that microglia activation states are
                      responsible for FDG-PET signal alterations in patients with
                      neurodegenerative diseases and mouse models for amyloidosis.
                      Microglial activation states should therefore be considered
                      when performing FDG-PET.},
      cin          = {INM-2},
      ddc          = {500},
      cid          = {I:(DE-Juel1)INM-2-20090406},
      pnm          = {5253 - Neuroimaging (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5253},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {34644146},
      UT           = {WOS:000707525800003},
      doi          = {10.1126/scitranslmed.abe5640},
      url          = {https://juser.fz-juelich.de/record/904376},
}