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@ARTICLE{Voelkl:259914,
      author       = {Voelkl, Kerstin and Gutiérrez-Ángel, Sara and Keeling,
                      Sophie and Koyuncu, Seda and da Silva Padilha, Miguel and
                      Feigenbutz, Dennis and Arzberger, Thomas and Vilchez, David
                      and Klein, Rüdiger and Dudanova, Irina},
      title        = {{N}europrotective effects of hepatoma-derived growth factor
                      in models of {H}untington's disease.},
      journal      = {Life science alliance},
      volume       = {6},
      number       = {11},
      issn         = {2575-1077},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DZNE-2023-00799},
      pages        = {e202302018},
      year         = {2023},
      abstract     = {Huntington's disease (HD) is a movement disorder caused by
                      a mutation in the Huntingtin gene that leads to severe
                      neurodegeneration. Molecular mechanisms of HD are not
                      sufficiently understood, and no cure is currently available.
                      Here, we demonstrate neuroprotective effects of
                      hepatoma-derived growth factor (HDGF) in cellular and mouse
                      HD models. We show that HD-vulnerable neurons in the
                      striatum and cortex express lower levels of HDGF than
                      resistant ones. Moreover, lack of endogenous HDGF
                      exacerbated motor impairments and reduced the life span of
                      R6/2 Huntington's disease mice. AAV-mediated delivery of
                      HDGF into the brain reduced mutant Huntingtin inclusion
                      load, but had no significant effect on motor behavior or
                      life span. Interestingly, both nuclear and cytoplasmic
                      versions of HDGF were efficient in rescuing mutant
                      Huntingtin toxicity in cellular HD models. Moreover,
                      extracellular application of recombinant HDGF improved
                      viability of mutant Huntingtin-expressing primary neurons
                      and reduced mutant Huntingtin aggregation in neural
                      progenitor cells differentiated from human patient-derived
                      induced pluripotent stem cells. Our findings provide new
                      insights into the pathomechanisms of HD and demonstrate
                      neuroprotective potential of HDGF in neurodegeneration.},
      keywords     = {Mice / Humans / Animals / Huntington Disease: genetics /
                      Huntington Disease: drug therapy / Huntington Disease:
                      metabolism / Neuroprotective Agents: pharmacology /
                      Neuroprotective Agents: metabolism / Neuroprotective Agents:
                      therapeutic use / Neurons: metabolism / Intercellular
                      Signaling Peptides and Proteins: metabolism /
                      Neuroprotective Agents (NLM Chemicals) / hepatoma-derived
                      growth factor (NLM Chemicals) / Intercellular Signaling
                      Peptides and Proteins (NLM Chemicals)},
      cin          = {Neuropathology / Brainbank},
      ddc          = {570},
      cid          = {I:(DE-2719)1140013},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC10427761},
      pubmed       = {pmid:37580082},
      doi          = {10.26508/lsa.202302018},
      url          = {https://pub.dzne.de/record/259914},
}