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@ARTICLE{Dunkelmann:840384,
      author       = {Dunkelmann, Tina and Teichmann, Kerstin and Ziehm, Tamar
                      and Schemmert, Sarah and Frenzel, Daniel and Tusche, Markus
                      and Dammers, Christina and Jürgens, Dagmar and Langen,
                      Karl-Josef and Demuth, Hans-Ulrich and Shah, N. J. and
                      Kutzsche, Janine and Willuweit, Antje and Willbold, Dieter},
      title        = {{A}β oligomer eliminating compounds interfere successfully
                      with p{EA}β (3–42) induced motor neurodegenerative
                      phenotype in transgenic mice},
      journal      = {Neuropeptides},
      volume       = {67},
      issn         = {0143-4179},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {FZJ-2017-07917},
      pages        = {27-35},
      year         = {2018},
      abstract     = {Currently, there are no causative or disease modifying
                      treatments available for Alzheimer's disease (AD).
                      Previously, it has been shown that D3, a small, fully
                      d-enantiomeric peptide is able to eliminate low molecular
                      weight Aβ oligomers in vitro, enhance cognition and reduce
                      plaque load in AD transgenic mice. To further characterise
                      the therapeutic potential of D3 towards N-terminally
                      truncated and pyroglutamated Aβ (pEAβ(3–42)) we tested
                      D3 and its head-to-tail tandem derivative D3D3 both in vitro
                      and in vivo in the new mouse model TBA2.1. These mice
                      produce human pEAβ(3–42) leading to a strong, early onset
                      motor neurodegenerative phenotype. In the present study, we
                      were able to demonstrate 1) strong binding affinity of both
                      D3 and D3D3 to pEAβ(3–42) in comparison to Aβ(1–42)
                      and 2) increased affinity of the tandem derivative D3D3 in
                      comparison to D3. Subsequently we tested the therapeutic
                      potentials of both peptides in the TBA2.1 animal model.
                      Truly therapeutic, non-preventive treatment with D3 and D3D3
                      clearly slowed the progression of the neurodegenerative
                      TBA2.1 phenotype, indicating the strong therapeutic
                      potential of both peptides against pEAβ(3–42) induced
                      neurodegeneration.},
      cin          = {ICS-6 / INM-4 / JARA-BRAIN},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-6-20110106 / I:(DE-Juel1)INM-4-20090406 /
                      $I:(DE-82)080010_20140620$},
      pnm          = {573 - Neuroimaging (POF3-573)},
      pid          = {G:(DE-HGF)POF3-573},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29273382},
      UT           = {WOS:000425556500004},
      doi          = {10.1016/j.npep.2017.11.011},
      url          = {https://juser.fz-juelich.de/record/840384},
}