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@ARTICLE{Ballweg:256590,
      author       = {Ballweg, Anna and Klaus, Carolin and Vogler, Letizia and
                      Katzdobler, Sabrina and Wind, Karin and Zatcepin, Artem and
                      Ziegler, Sibylle I and Secgin, Birkan and Eckenweber,
                      Florian and Bohr, Bernd and Bernhardt, Maximilian Alexander
                      and Fietzek, Urban and Rauchmann, Boris-Stephan and
                      Stoecklein, Sophia and Quach, Stefanie and Beyer, Leonie and
                      Scheifele, Maximilian and Simmet, Marcel and Joseph, Emanuel
                      and Lindner, Simon and Berg, Isabella and Koglin, Norman and
                      Mueller, Andre and Stephens, Andrew W and Bartenstein, Peter
                      and Tonn, Joerg C and Albert, Nathalie L and Kümpfel, Tania
                      and Kerschensteiner, Martin and Perneczky, Robert and Levin,
                      Johannes and Paeger, Lars and Herms, Jochen and Brendel,
                      Matthias},
      title        = {[18{F}]{F}-{DED} {PET} imaging of reactive astrogliosis in
                      neurodegenerative diseases: preclinical proof of concept and
                      first-in-human data.},
      journal      = {Journal of neuroinflammation},
      volume       = {20},
      number       = {1},
      issn         = {1742-2094},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DZNE-2023-00348},
      pages        = {68},
      year         = {2023},
      note         = {CC BY},
      abstract     = {Reactive gliosis is a common pathological hallmark of CNS
                      pathology resulting from neurodegeneration and
                      neuroinflammation. In this study we investigate the
                      capability of a novel monoamine oxidase B (MAO-B) PET ligand
                      to monitor reactive astrogliosis in a transgenic mouse model
                      of Alzheimer`s disease (AD). Furthermore, we performed a
                      pilot study in patients with a range of neurodegenerative
                      and neuroinflammatory conditions.A cross-sectional cohort of
                      24 transgenic (PS2APP) and 25 wild-type mice (age range:
                      4.3-21.0 months) underwent 60 min dynamic
                      [18F]fluorodeprenyl-D2 ([18F]F-DED), static 18 kDa
                      translocator protein (TSPO, [18F]GE-180) and β-amyloid
                      ([18F]florbetaben) PET imaging. Quantification was performed
                      via image derived input function (IDIF, cardiac input),
                      simplified non-invasive reference tissue modelling (SRTM2,
                      DVR) and late-phase standardized uptake value ratios (SUVr).
                      Immunohistochemical (IHC) analyses of glial fibrillary
                      acidic protein (GFAP) and MAO-B were performed to validate
                      PET imaging by gold standard assessments. Patients belonging
                      to the Alzheimer's disease continuum (AD, n = 2),
                      Parkinson's disease (PD, n = 2), multiple system atrophy
                      (MSA, n = 2), autoimmune encephalitis (n = 1),
                      oligodendroglioma (n = 1) and one healthy control underwent
                      60 min dynamic [18F]F-DED PET and the data were analyzed
                      using equivalent quantification strategies.We selected the
                      cerebellum as a pseudo-reference region based on the
                      immunohistochemical comparison of age-matched PS2APP and WT
                      mice. Subsequent PET imaging revealed that PS2APP mice
                      showed elevated hippocampal and thalamic [18F]F-DED DVR when
                      compared to age-matched WT mice at 5 months (thalamus: +
                      $4.3\%;$ p = 0.048), 13 months (hippocampus: + $7.6\%,$ p =
                      0.022) and 19 months (hippocampus: + $12.3\%,$ p < 0.0001;
                      thalamus: + $15.2\%,$ p < 0.0001). Specific [18F]F-DED DVR
                      increases of PS2APP mice occurred earlier when compared to
                      signal alterations in TSPO and β-amyloid PET and [18F]F-DED
                      DVR correlated with quantitative immunohistochemistry
                      (hippocampus: R = 0.720, p < 0.001; thalamus: R = 0.727, p =
                      0.002). Preliminary experience in patients showed [18F]F-DED
                      VT and SUVr patterns, matching the expected topology of
                      reactive astrogliosis in neurodegenerative (MSA) and
                      neuroinflammatory conditions, whereas the patient with
                      oligodendroglioma and the healthy control indicated
                      [18F]F-DED binding following the known physiological MAO-B
                      expression in brain.[18F]F-DED PET imaging is a promising
                      approach to assess reactive astrogliosis in AD mouse models
                      and patients with neurological diseases.},
      keywords     = {Humans / Mice / Animals / Infant / Gliosis: pathology /
                      Neurodegenerative Diseases: metabolism / Oligodendroglioma:
                      metabolism / Oligodendroglioma: pathology / Cross-Sectional
                      Studies / Pilot Projects / Alzheimer Disease: pathology /
                      Positron-Emission Tomography: methods / Amyloid
                      beta-Peptides: metabolism / Brain: metabolism / Mice,
                      Transgenic / Inflammation: metabolism / Monoamine Oxidase:
                      metabolism / Receptors, GABA: metabolism / Astrocytes
                      (Other) / Deprenyl (Other) / MAO-B (Other) / PET (Other) /
                      Amyloid beta-Peptides (NLM Chemicals) / Monoamine Oxidase
                      (NLM Chemicals) / TSPO protein, human (NLM Chemicals) /
                      Receptors, GABA (NLM Chemicals)},
      cin          = {AG Haass old / AG Herms / AG Dichgans / Clinical Dementia
                      Research München},
      ddc          = {610},
      cid          = {I:(DE-2719)1110007 / I:(DE-2719)1110001 /
                      I:(DE-2719)5000022 / I:(DE-2719)1111016},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
                      Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36906584},
      pmc          = {pmc:PMC10007845},
      doi          = {10.1186/s12974-023-02749-2},
      url          = {https://pub.dzne.de/record/256590},
}