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@ARTICLE{Jhrling:137945,
      author       = {Jährling, Nina and Becker, Klaus and Wegenast-Braun,
                      Bettina M and Grathwohl, Stefan A and Jucker, Mathias and
                      Dodt, Hans-Ulrich},
      title        = {{C}erebral β-{A}myloidosis in {M}ice {I}nvestigated by
                      {U}ltramicroscopy.},
      journal      = {PLOS ONE},
      volume       = {10},
      number       = {5},
      issn         = {1932-6203},
      address      = {San Francisco, California, US},
      publisher    = {PLOS},
      reportid     = {DZNE-2020-04267},
      pages        = {e0125418},
      year         = {2015},
      abstract     = {Alzheimer´s disease (AD) is the most common
                      neurodegenerative disorder. AD neuropathology is
                      characterized by intracellular neurofibrillary tangles and
                      extracellular β-amyloid deposits in the brain. To elucidate
                      the complexity of AD pathogenesis a variety of transgenic
                      mouse models have been generated. An ideal imaging system
                      for monitoring β-amyloid plaque deposition in the brain of
                      these animals should allow 3D-reconstructions of β-amyloid
                      plaques via a single scan of an uncropped brain.
                      Ultramicroscopy makes this possible by replacing mechanical
                      slicing in standard histology by optical sectioning. It
                      allows a time efficient analysis of the amyloid plaque
                      distribution in the entire mouse brain with 3D cellular
                      resolution. We herein labeled β-amyloid deposits in a
                      transgenic mouse model of cerebral β-amyloidosis (APPPS1
                      transgenic mice) with two intraperitoneal injections of the
                      amyloid-binding fluorescent dye methoxy-X04. Upon postmortem
                      analysis the total number of β-amyloid plaques, the
                      β-amyloid load (volume percent) and the amyloid plaque size
                      distributions were measured in the frontal cortex of two age
                      groups (2.5 versus 7-8.5 month old mice). Applying
                      ultramicroscopy we found in a proof-of-principle study that
                      the number of β-amyloid plaques increases with age. In our
                      experiments we further observed an increase of large plaques
                      in the older age group of mice. We demonstrate that
                      ultramicroscopy is a fast, and accurate analysis technique
                      for studying β-amyloid lesions in transgenic mice allowing
                      the 3D staging of β-amyloid plaque development. This in
                      turn is the basis to study neural network degeneration upon
                      cerebral β-amyloidosis and to assess Aβ-targeting
                      therapeutics.},
      keywords     = {Alkenes: analysis / Alkenes: metabolism / Amyloid
                      beta-Protein Precursor: genetics / Amyloidosis: pathology /
                      Animals / Benzene Derivatives: analysis / Benzene
                      Derivatives: metabolism / Brain: pathology / Disease Models,
                      Animal / Fluorescent Dyes: analysis / Fluorescent Dyes:
                      metabolism / Humans / Imaging, Three-Dimensional: methods /
                      Mice, Inbred C57BL / Mice, Transgenic / Microscopy: methods
                      / Plaque, Amyloid: pathology / Stilbenes /
                      1,4-bis(4'-hydroxystyryl)-2-methoxybenzene (NLM Chemicals) /
                      Alkenes (NLM Chemicals) / Amyloid beta-Protein Precursor
                      (NLM Chemicals) / Benzene Derivatives (NLM Chemicals) /
                      Fluorescent Dyes (NLM Chemicals) / Stilbenes (NLM
                      Chemicals)},
      cin          = {AG Jucker},
      ddc          = {610},
      cid          = {I:(DE-2719)1210001},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26017149},
      pmc          = {pmc:PMC4446269},
      doi          = {10.1371/journal.pone.0125418},
      url          = {https://pub.dzne.de/record/137945},
}