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@ARTICLE{vanGroen:840658,
      author       = {van Groen, Thomas and Schemmert, Sarah and Brener,
                      Oleksandr and Gremer, Lothar and Ziehm, Tamar and Tusche,
                      Markus and Nagel-Steger, Luitgard and Kadish, Inga and
                      Schartmann, Elena and Elfgen, Anne and Jürgens, Dagmar and
                      Willuweit, Antje and Kutzsche, Janine and Willbold, Dieter},
      title        = {{T}he {A}β oligomer eliminating {D}-enantiomeric peptide
                      {RD}2 improves cognition without changing plaque pathology},
      journal      = {Scientific reports},
      volume       = {7},
      number       = {1},
      issn         = {2045-2322},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {FZJ-2017-08159},
      pages        = {16275},
      year         = {2017},
      abstract     = {While amyloid-β protein (Aβ) aggregation into insoluble
                      plaques is one of the pathological hallmarks of
                      Alzheimer’s disease (AD), soluble oligomeric Aβ has been
                      hypothesized to be responsible for synapse damage,
                      neurodegeneration, learning, and memory deficits in AD.
                      Here, we investigate the in vitro and in vivo efficacy of
                      the d-enantiomeric peptide RD2, a rationally designed
                      derivative of the previously described lead compound D3,
                      which has been developed to efficiently eliminate toxic
                      Aβ42 oligomers as a promising treatment strategy for AD.
                      Besides the detailed in vitro characterization of RD2, we
                      also report the results of a treatment study of APP/PS1 mice
                      with RD2. After 28 days of treatment we observed enhancement
                      of cognition and learning behaviour. Analysis on brain
                      plaque load did not reveal significant changes, but a
                      significant reduction of insoluble Aβ42. Our findings
                      demonstrate that RD2 was significantly more efficient in Aβ
                      oligomer elimination in vitro compared to D3. Enhanced
                      cognition without reduction of plaque pathology in parallel
                      suggests that synaptic malfunction due to Aβ oligomers
                      rather than plaque pathology is decisive for disease
                      development and progression. Thus, Aβ oligomer elimination
                      by RD2 treatment may be also beneficial for AD patients.},
      cin          = {ICS-6 / INM-4},
      ddc          = {000},
      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},
      UT           = {WOS:000416135000074},
      pubmed       = {pmid:29176708},
      doi          = {10.1038/s41598-017-16565-1},
      url          = {https://juser.fz-juelich.de/record/840658},
}