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@ARTICLE{Schemmert:857061,
      author       = {Schemmert, Sarah and Schartmann, Elena and Honold, Dominik
                      and Zafiu, Christian and Ziehm, Tamar and Langen, Karl-Josef
                      and Shah, Nadim Joni and Kutzsche, Janine and Willuweit,
                      Antje and Willbold, Dieter},
      title        = {{D}eceleration of the neurodegenerative phenotype in
                      pyroglutamate-{A}β accumulating transgenic mice by oral
                      treatment with the {A}β oligomer eliminating compound
                      {RD}2},
      journal      = {Neurobiology of disease},
      volume       = {124},
      issn         = {0969-9961},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {FZJ-2018-06329},
      pages        = {36-45},
      year         = {2019},
      abstract     = {Alzheimer's disease, a multifactorial incurable disorder,
                      is mainly characterised by progressive neurodegeneration,
                      extracellular accumulation of amyloid-β protein (Aβ), and
                      intracellular aggregation of hyperphosphorylated tau
                      protein. During the last years, Aβ oligomers have been
                      claimed to be the disease causing agent. Consequently,
                      development of compounds that are able to disrupt already
                      existing Aβ oligomers is highly desirable. We developed
                      d-enantiomeric peptides, consisting solely of d-enantiomeric
                      amino acid residues, for the direct and specific elimination
                      of toxic Aβ oligomers. The drug candidate RD2 did show high
                      oligomer elimination efficacy in vitro and the in vivo
                      efficacy of RD2 was demonstrated in treatment studies by
                      enhanced cognition in transgenic mouse models of
                      amyloidosis. Here, we report on the in vitro and in vivo
                      efficacy of the compound towards pyroglutamate-Aβ, a
                      particular aggressive Aβ species. Using the transgenic
                      TBA2.1 mouse model, which develops pyroglutamate-Aβ(3–42)
                      induced neurodegeneration, we are able to show that oral RD2
                      treatment resulted in a significant deceleration of the
                      progression of the phenotype. The in vivo efficacy against
                      this highly toxic Aβ species further validates RD2 as a
                      drug candidate for the therapeutic use in humans.},
      cin          = {ICS-6 / INM-4},
      ddc          = {570},
      cid          = {I:(DE-Juel1)ICS-6-20110106 / I:(DE-Juel1)INM-4-20090406},
      pnm          = {553 - Physical Basis of Diseases (POF3-553)},
      pid          = {G:(DE-HGF)POF3-553},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30391539},
      UT           = {WOS:000459217800004},
      doi          = {10.1016/j.nbd.2018.10.021},
      url          = {https://juser.fz-juelich.de/record/857061},
}