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@ARTICLE{Willuweit:897431,
      author       = {Willuweit, Antje and Schöneck, Michael and Schemmert,
                      Sarah and Lohmann, Philipp and Bremen, Saskia and Honold,
                      Dominik and Burda, Nicole and Jiang, Nan and Beer, Simone
                      and Ermert, Johannes and Willbold, Dieter and Shah, N. Jon
                      and Langen, Karl-Josef},
      title        = {{C}omparison of the {A}myloid {L}oad in the {B}rains of
                      {T}wo {T}ransgenic {A}lzheimer’s {D}isease {M}ouse
                      {M}odels {Q}uantified by {F}lorbetaben {P}ositron {E}mission
                      {T}omography},
      journal      = {Frontiers in neuroscience},
      volume       = {15},
      issn         = {1662-453X},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {FZJ-2021-03785},
      pages        = {699926},
      year         = {2021},
      abstract     = {Alzheimer’s disease (AD) is characterized by formation of
                      amyloid plaques and neurofibrillary tangles in the brain,
                      which can be mimicked by transgenic mouse models. Here, we
                      report on the characterization of amyloid load in the brains
                      of two transgenic amyloidosis models using positron emission
                      tomography (PET) with florbetaben (FBB), an 18F-labeled
                      amyloid PET tracer routinely used in AD patients. Young,
                      middle-aged, and old homozygous APP/PS1 mice (ARTE10), old
                      hemizygous APPswe/PS1ΔE9, and old wild-type control mice
                      were subjected to FBB PET using a small animal PET/computed
                      tomography scanner. After PET, brains were excised, and ex
                      vivo autoradiography was performed. Plaque pathology was
                      verified on brain sections with histological methods.
                      Amyloid plaque load increased progressively with age in the
                      cortex and hippocampus of ARTE10 mice, which could be
                      detected with both in vivo FBB PET and ex vivo
                      autoradiography. FBB retention showed significant
                      differences to wild-type controls already at 9 months of age
                      by both in vivo and ex vivo analyses. An excellent
                      correlation between data derived from PET and
                      autoradiography could be obtained (rPearson = 0.947, p <
                      0.0001). Although amyloid load detected by FBB in the brains
                      of old APPswe/PS1ΔE9 mice was as low as values obtained
                      with young ARTE10 mice, statistically significant
                      discrimination to wild-type animals was reached (p < 0.01).
                      In comparison to amyloid burden quantified by histological
                      analysis, FBB retention correlated best with total plaque
                      load and number of congophilic plaques in the brains of both
                      mouse models. In conclusion, the homozygous ARTE10 mouse
                      model showed superior properties over APPswe/PS1ΔE9 mice
                      for FBB small animal amyloid PET imaging. The absolute
                      amount of congophilic dense-cored plaques seems to be the
                      decisive factor for feasibility of amyloidosis models for
                      amyloid PET analysis.},
      cin          = {INM-4 / INM-11 / JARA-BRAIN / IBI-7 / INM-2 / INM-5},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-4-20090406 / I:(DE-Juel1)INM-11-20170113 /
                      I:(DE-Juel1)VDB1046 / I:(DE-Juel1)IBI-7-20200312 /
                      I:(DE-Juel1)INM-2-20090406 / I:(DE-Juel1)INM-5-20090406},
      pnm          = {5253 - Neuroimaging (POF4-525) / 5244 - Information
                      Processing in Neuronal Networks (POF4-524)},
      pid          = {G:(DE-HGF)POF4-5253 / G:(DE-HGF)POF4-5244},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {34671235},
      UT           = {WOS:000717045000001},
      doi          = {10.3389/fnins.2021.699926},
      url          = {https://juser.fz-juelich.de/record/897431},
}