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@ARTICLE{Camargo:893764,
      author       = {Camargo, Luana and Schöneck, Michael and Sangarapillai,
                      Nivethini and Honold, Dominik and Shah, N. J. and Langen,
                      Karl-Josef and Willbold, Dieter and Kutzsche, Janine and
                      Schemmert, Sarah and Willuweit, Antje},
      title        = {{PEA}β {T}riggers {C}ognitive {D}ecline and {A}myloid
                      {B}urden in a {N}ovel {M}ouse {M}odel of {A}lzheimer’s
                      {D}isease},
      journal      = {International journal of molecular sciences},
      volume       = {22},
      number       = {13},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {FZJ-2021-02819},
      pages        = {7062 -},
      year         = {2021},
      abstract     = {Understanding the physiopathology of Alzheimer’s disease
                      (AD) has improved substantially based on studies of mouse
                      models mimicking at least one aspect of the disease. Many
                      transgenic lines have been established, leading to
                      amyloidosis but lacking neurodegeneration. The aim of the
                      current study was to generate a novel mouse model that
                      develops neuritic plaques containing the aggressive
                      pyroglutamate modified amyloid-β (pEAβ) species in the
                      brain. The TAPS line was developed by intercrossing of the
                      pEAβ-producing TBA2.1 mice with the plaque-developing line
                      APPswe/PS1ΔE9. The phenotype of the new mouse line was
                      characterized using immunostaining, and different cognitive
                      and general behavioral tests. In comparison to the parental
                      lines, TAPS animals developed an earlier onset of pathology
                      and increased plaque load, including striatal pEAβ-positive
                      neuritic plaques, and enhanced neuroinflammation. In
                      addition to abnormalities in general behavior, locomotion,
                      and exploratory behavior, TAPS mice displayed cognitive
                      deficits in a variety of tests that were most pronounced in
                      the fear conditioning paradigm and in spatial learning in
                      comparison to the parental lines. In conclusion, the
                      combination of a pEAβ- and a plaque-developing mouse model
                      led to an accelerated amyloid pathology and cognitive
                      decline in TAPS mice, qualifying this line as a novel
                      amyloidosis model for future studies.},
      cin          = {IBI-7 / INM-4 / JARA-BRAIN},
      ddc          = {540},
      cid          = {I:(DE-Juel1)IBI-7-20200312 / I:(DE-Juel1)INM-4-20090406 /
                      I:(DE-Juel1)VDB1046},
      pnm          = {5252 - Brain Dysfunction and Plasticity (POF4-525) / 5244 -
                      Information Processing in Neuronal Networks (POF4-524)},
      pid          = {G:(DE-HGF)POF4-5252 / G:(DE-HGF)POF4-5244},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {34209113},
      UT           = {WOS:000671201600001},
      doi          = {10.3390/ijms22137062},
      url          = {https://juser.fz-juelich.de/record/893764},
}