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@ARTICLE{Post:891058,
      author       = {Post, Julia and Kogel, Vanessa and Schaffrath, Anja and
                      Lohmann, Philipp and Shah, N. J. and Langen, Karl-Josef and
                      Willbold, Dieter and Willuweit, Antje and Kutzsche, Janine},
      title        = {{A} {N}ovel {A}nti-{I}nflammatory d-{P}eptide {I}nhibits
                      {D}isease {P}henotype {P}rogression in an {ALS} {M}ouse
                      {M}odel},
      journal      = {Molecules},
      volume       = {26},
      number       = {6},
      issn         = {1420-3049},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {FZJ-2021-01341},
      pages        = {1590 -},
      year         = {2021},
      abstract     = {Amyotrophic lateral sclerosis (ALS) is a progressive
                      neurodegenerative disease characterised by selective
                      neuronal death in the brain stem and spinal cord. The cause
                      is unknown, but an increasing amount of evidence has firmly
                      certified that neuroinflammation plays a key role in ALS
                      pathogenesis. Neuroinflammation is a pathological hallmark
                      of several neurodegenerative disorders and has been
                      implicated as driver of disease progression. Here, we
                      describe a treatment study demonstrating the therapeutic
                      potential of a tandem version of the well-known
                      all-d-peptide RD2 (RD2RD2) in a transgenic mouse model of
                      ALS (SOD1*G93A). Mice were treated intraperitoneally for
                      four weeks with RD2RD2 vs. placebo. SOD1*G93A mice were
                      tested longitudinally during treatment in various
                      behavioural and motor coordination tests. Brain and spinal
                      cord samples were investigated immunohistochemically for
                      gliosis and neurodegeneration. RD2RD2 treatment in SOD1*G93A
                      mice resulted not only in a reduction of activated
                      astrocytes and microglia in both the brain stem and lumbar
                      spinal cord, but also in a rescue of neurons in the motor
                      cortex. RD2RD2 treatment was able to slow progression of the
                      disease phenotype, especially the motor deficits, to an
                      extent that during the four weeks treatment duration, no
                      significant progression was observed in any of the motor
                      experiments. Based on the presented results, we conclude
                      that RD2RD2 is a potential therapeutic candidate against
                      ALS.},
      cin          = {IBI-7 / INM-4 / INM-11 / JARA-BRAIN},
      ddc          = {540},
      cid          = {I:(DE-Juel1)IBI-7-20200312 / I:(DE-Juel1)INM-4-20090406 /
                      I:(DE-Juel1)INM-11-20170113 / I:(DE-Juel1)VDB1046},
      pnm          = {525 - Decoding Brain Organization and Dysfunction
                      (POF4-525) / 5244 - Information Processing in Neuronal
                      Networks (POF4-524)},
      pid          = {G:(DE-HGF)POF4-525 / G:(DE-HGF)POF4-5244},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {33805709},
      UT           = {WOS:000645434200001},
      doi          = {10.3390/molecules26061590},
      url          = {https://juser.fz-juelich.de/record/891058},
}