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@ARTICLE{Schemmert:850919,
      author       = {Schemmert, Sarah and Schartmann, Elena and Zafiu, Christian
                      and Kass, Bettina and Hartwig, Sonja and Lehr, Stefan and
                      Bannach, Oliver and Langen, Karl-Josef and Shah, Nadim Joni
                      and Kutzsche, Janine and Willuweit, Antje and Willbold,
                      Dieter},
      title        = {{A}β {O}ligomer {E}limination {R}estores {C}ognition in
                      {T}ransgenic {A}lzheimer’s {M}ice with {F}ull-blown
                      {P}athology},
      journal      = {Molecular neurobiology},
      volume       = {56},
      number       = {3},
      issn         = {0893-7648},
      address      = {Totowa, NJ},
      publisher    = {Humana Press},
      reportid     = {FZJ-2018-04653},
      pages        = {2211-2223},
      year         = {2019},
      abstract     = {Oligomers of the amyloid-β (Aβ) protein are suspected to
                      be responsible for the development and progression of
                      Alzheimer’s disease. Thus, the development of compounds
                      that are able to eliminate already formed toxic Aβ
                      oligomers is very desirable. Here, we describe the in vivo
                      efficacy of the compound RD2, which was developed to
                      directly and specifically eliminate toxic Aβ oligomers. In
                      a truly therapeutic, rather than a preventive study, oral
                      treatment with RD2 was able to reverse cognitive deficits
                      and significantly reduce Aβ pathology in old-aged
                      transgenic Alzheimer’s Disease mice with full-blown
                      pathology and behavioral deficits. For the first time, we
                      demonstrate the in vivo target engagement of RD2 by showing
                      a significant reduction of Aβ oligomers in the brains of
                      RD2-treated mice compared to placebo-treated mice. The
                      correlation of Aβ elimination in vivo and the reversal of
                      cognitive deficits in old-aged transgenic mice support the
                      hypothesis that Aβ oligomers are relevant not only for
                      disease development and progression, but also offer a
                      promising target for the causal treatment of Alzheimer’s
                      disease.},
      cin          = {ICS-6 / INM-4 / INM-11 / JARA-BRAIN},
      ddc          = {570},
      cid          = {I:(DE-Juel1)ICS-6-20110106 / I:(DE-Juel1)INM-4-20090406 /
                      I:(DE-Juel1)INM-11-20170113 / $I:(DE-82)080010_20140620$},
      pnm          = {553 - Physical Basis of Diseases (POF3-553)},
      pid          = {G:(DE-HGF)POF3-553},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30003517},
      UT           = {WOS:000460163700049},
      doi          = {10.1007/s12035-018-1209-3},
      url          = {https://juser.fz-juelich.de/record/850919},
}