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@MISC{Xie:285639,
      author       = {Xie, Kan and Ryan, Devon and Bonn, Stefan and Ehninger,
                      Dan},
      title        = {{D}ataset: {O}ver-expression of human mutated {APP}
                      transgene in the mouse brain induces differential gene
                      expression profiles depending on the age of exposure},
      publisher    = {Gene Expression Omnibus},
      reportid     = {DZNE-2026-00278},
      year         = {2026},
      abstract     = {Alzheimer's disease (AD) is the most prevalent
                      neurodegenerative disorder causing about two third of all
                      dementia cases in the elderly. Although AD pathological
                      features have been intensively examined in numerous
                      scientific studies employing invertebrate and vertebrate
                      model organisms, the exact underlying mechanisms remain
                      poorly understood. Extracellular accumulation of amyloid
                      beta (Aβ) peptides represents a pathological hallmark of AD
                      and it has been considered as the initiation point of AD by
                      the popular amyloid hypothesis. In the current study, we aim
                      to address whether expression of a mutated APP transgene
                      (APPSweInd) would provoke differential neurological outcomes
                      depending on the age of exposure in mice. Towards this end,
                      we employed a tetracycline-based inducible genetic system to
                      target APPSweInd transgene expression to defined age
                      intervals initiated at adulthood, i.e., between 6-18 months
                      (= mid-aged group) and 12-24 months (= aged group).
                      Surprisingly, over-expression of mutant APP reduced the
                      transcriptional levels of genes embedded in the cholinergic
                      network exclusively in the aged mouse brain, while gene
                      expression profiles related to inflammatory activation and
                      exacerbated gliosis were shared between age groups. Hence,
                      our data support the notion that AD pathology may rely on a
                      disruption of the cholinergic system that is triggered
                      through an altered response of the aged brain towards toxic
                      Aβ aggregates.},
      cin          = {AG Ehninger},
      cid          = {I:(DE-2719)1013005},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)32},
      url          = {https://pub.dzne.de/record/285639},
}