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@ARTICLE{Wintz:1007370,
      author       = {Wintz, Katharina and Post, Julia and Langen, Karl-Josef and
                      Willbold, Dieter and Willuweit, Antje and Kutzsche, Janine},
      title        = {{O}ral {T}reatment with d-{RD}2{RD}2 {I}mpedes {E}arly
                      {D}isease {M}echanisms in {SOD}1*{G}93{A} {T}ransgenic
                      {M}ice but {D}oes {N}ot {P}rolong {S}urvival},
      journal      = {Biomedicines},
      volume       = {11},
      number       = {4},
      issn         = {2227-9059},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {FZJ-2023-02035},
      pages        = {995 -},
      year         = {2023},
      abstract     = {Amyotrophic lateral sclerosis (ALS) is a neurodegenerative
                      disease affecting upper and lower motor neurons, thus,
                      progressing to complete muscle loss until the patient dies
                      from respiratory arrest. The disease is not curable, and
                      patients die approximately 2–5 years after diagnosis.
                      Studying the underlying disease mechanisms to get access to
                      new treatment options is, therefore, essential for
                      patients’ benefit. However, so far, only three drugs that
                      alleviate the symptoms have been approved by the U.S. Food
                      and Drug Administration (FDA). A new drug candidate for the
                      treatment of ALS is the all-d-enantiomeric peptide RD2RD2.
                      In this study, we investigated the therapeutic effect of
                      RD2RD2 in two setups. First, we analyzed disease progression
                      and survival in 7 week-old B6.Cg-Tg(SOD1*G93A)1Gur/J mice.
                      Second, we confirmed the result of the survival analysis in
                      the B6SJL-Tg(SOD1*G93A)1Gur/J mouse line. Shortly before
                      disease onset, the mice were treated daily with an oral dose
                      of 50 mg/kg body weight. Treatment with RD2RD2 led to a
                      delayed disease onset and reduced motor phenotype as shown
                      using the SHIRPA test, the splay reflex test, and the pole
                      test, but did not affect survival. In conclusion, RD2RD2 has
                      the ability to delay the onset of symptoms.},
      cin          = {IBI-7 / INM-4},
      ddc          = {570},
      cid          = {I:(DE-Juel1)IBI-7-20200312 / I:(DE-Juel1)INM-4-20090406},
      pnm          = {5244 - Information Processing in Neuronal Networks
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-5244},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {37189613},
      UT           = {WOS:000977211400001},
      doi          = {10.3390/biomedicines11040995},
      url          = {https://juser.fz-juelich.de/record/1007370},
}