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@ARTICLE{Dunkelmann:842478,
      author       = {Dunkelmann, Tina and Schemmert, Sarah and Honold, Dominik
                      and Teichmann, Kerstin and Butzküven, Elke and Demuth,
                      Hans-Ulrich and Shah, N. J. and Langen, Karl-Josef and
                      Kutzsche, Janine and Willbold, Dieter and Willuweit, Antje},
      title        = {{C}omprehensive characterization of the pyroglutamate {A}β
                      induced motor neurodegenerative phenotype of {TBA}2.1 mice},
      journal      = {Journal of Alzheimer's disease},
      volume       = {63},
      number       = {1},
      issn         = {1387-2877},
      address      = {Amsterdam},
      publisher    = {IOS Press},
      reportid     = {FZJ-2018-00703},
      pages        = {115-130},
      year         = {2018},
      abstract     = {Alzheimer’s disease (AD) is the most common
                      neurodegenerative disorder and is being intensively
                      investigated using a broad variety of animal models. Many of
                      these models express mutant versions of human amyloid-β
                      protein precursor (AβPP) that are associated with
                      amyloid-β protein (Aβ)-induced early onset familial AD.
                      Most of these models, however, do not develop bold
                      neurodegenerative pathology and the respective phenotypes.
                      Nevertheless, this may well be essential for their
                      suitability to identify therapeutically active compounds
                      that have the potential for a curative or at least
                      disease-modifying therapy in humans. In this study, the new
                      transgenic mouse model TBA2.1 was explored in detail to
                      increase knowledge about the neurodegenerative process
                      induced by the presence of pyroglutamate modified human
                      Aβ3-42 (pEAβ3-42). Analysis of the sensorimotor phenotype,
                      motor coordination, Aβ pathology, neurodegeneration, and
                      gliosis revealed formation and progression of severe
                      pathology and phenotypes including massive neuronal loss in
                      homozygous TBA2.1 mice within a few months. In contrast, the
                      start of a slight phenotype was observed only after 21
                      months in heterozygous mice. These data highlight the role
                      of pEAβ3-42 in the disease development and progression of
                      AD. Based on the findings of this study, homozygous TBA2.1
                      mice can be utilized to gain deeper understanding in the
                      underlying mechanisms of pEAβ3-42 and might be suitable as
                      an animal model for treatment studies targeting toxic Aβ
                      species, complementary to the well described transgenic
                      AβPP mouse models.},
      cin          = {ICS-6 / INM-4 / JARA-BRAIN / INM-11},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-6-20110106 / I:(DE-Juel1)INM-4-20090406 /
                      $I:(DE-82)080010_20140620$ / I:(DE-Juel1)INM-11-20170113},
      pnm          = {573 - Neuroimaging (POF3-573) / 553 - Physical Basis of
                      Diseases (POF3-553)},
      pid          = {G:(DE-HGF)POF3-573 / G:(DE-HGF)POF3-553},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29578479},
      UT           = {WOS:000430016100011},
      doi          = {10.3233/JAD-170775},
      url          = {https://juser.fz-juelich.de/record/842478},
}