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@ARTICLE{Post:894073,
      author       = {Post, Julia and Schaffrath, Anja and Gering, Ian and
                      Hartwig, Sonja and Lehr, Stefan and Shah, N. J. and Langen,
                      Karl-Josef and Willbold, Dieter and Kutzsche, Janine and
                      Willuweit, Antje},
      title        = {{O}ral {T}reatment with {RD}2{RD}2 {I}mpedes {D}evelopment
                      of {M}otoric {P}henotype and {D}elays {S}ymptom {O}nset in
                      {SOD}1{G}93{A} {T}ransgenic {M}ice},
      journal      = {International journal of molecular sciences},
      volume       = {22},
      number       = {13},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {FZJ-2021-03023},
      pages        = {7066 -},
      year         = {2021},
      abstract     = {Neuroinflammation is a pathological hallmark of several
                      neurodegenerative disorders and plays a key role in the
                      pathogenesis of amyotrophic lateral sclerosis (ALS). It has
                      been implicated as driver of disease progression and is
                      observed in ALS patients, as well as in the transgenic
                      SOD1G93A mouse model. Here, we explore and validate the
                      therapeutic potential of the d-enantiomeric peptide RD2RD2
                      upon oral administration in SOD1G93A mice. Transgenic mice
                      were treated daily with RD2RD2 or placebo for 10 weeks and
                      phenotype progression was followed with several behavioural
                      tests. At the end of the study, plasma cytokine levels and
                      glia cell markers in brain and spinal cord were analysed.
                      Treatment resulted in a significantly increased performance
                      in behavioural and motor coordination tests and a
                      decelerated neurodegenerative phenotype in RD2RD2-treated
                      SOD1G93A mice. Additionally, we observed retardation of the
                      average disease onset. Treatment of SOD1G93A mice led to
                      significant reduction in glial cell activation and a rescue
                      of neurons. Analysis of plasma revealed normalisation of
                      several cytokines in samples of RD2RD2-treated SOD1G93A mice
                      towards the levels of non-transgenic mice. In conclusion,
                      these findings qualify RD2RD2 to be considered for further
                      development and testing towards a disease modifying ALS
                      treatment.},
      cin          = {INM-4 / INM-11 / JARA-BRAIN / IBI-7},
      ddc          = {540},
      cid          = {I:(DE-Juel1)INM-4-20090406 / I:(DE-Juel1)INM-11-20170113 /
                      I:(DE-Juel1)VDB1046 / I:(DE-Juel1)IBI-7-20200312},
      pnm          = {354 - Disease Prevention and Healthy Aging (POF4-354) /
                      5244 - Information Processing in Neuronal Networks
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-354 / G:(DE-HGF)POF4-5244},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {34209129},
      UT           = {WOS:000671088200001},
      doi          = {10.3390/ijms22137066},
      url          = {https://juser.fz-juelich.de/record/894073},
}