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@ARTICLE{Vlkner:258099,
      author       = {Völkner, Manuela and Wagner, Felix and Kurth, Thomas and
                      Sykes, Alex M and Del Toro Runzer, Claudia and Ebner, Lynn J
                      A and Kavak, Cagri and Alexaki, Vasileia Ismini and Cimalla,
                      Peter and Mehner, Mirko and Koch, Edmund and Karl, Mike O},
      title        = {{M}odeling inducible neuropathologies of the retina with
                      differential phenotypes in organoids.},
      journal      = {Frontiers in cellular neuroscience},
      volume       = {17},
      issn         = {1662-5102},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {DZNE-2023-00561},
      pages        = {1106287},
      year         = {2023},
      abstract     = {Neurodegenerative diseases remain incompletely understood
                      and therapies are needed. Stem cell-derived organoid models
                      facilitate fundamental and translational medicine research.
                      However, to which extent differential neuronal and glial
                      pathologic processes can be reproduced in current systems is
                      still unclear. Here, we tested 16 different chemical,
                      physical, and cell functional manipulations in mouse retina
                      organoids to further explore this. Some of the treatments
                      induce differential phenotypes, indicating that organoids
                      are competent to reproduce distinct pathologic processes.
                      Notably, mouse retina organoids even reproduce a complex
                      pathology phenotype with combined photoreceptor
                      neurodegeneration and glial pathologies upon combined (not
                      single) application of HBEGF and TNF, two factors previously
                      associated with neurodegenerative diseases. Pharmacological
                      inhibitors for MAPK signaling completely prevent
                      photoreceptor and glial pathologies, while inhibitors for
                      Rho/ROCK, NFkB, and CDK4 differentially affect them. In
                      conclusion, mouse retina organoids facilitate reproduction
                      of distinct and complex pathologies, mechanistic access,
                      insights for further organoid optimization, and modeling of
                      differential phenotypes for future applications in
                      fundamental and translational medicine research.},
      keywords     = {glia (Other) / mouse embryonic stem (mES) cells (Other) /
                      mouse organoid (Other) / neurodegeneration (Other) / neuron
                      (Other) / pathology modeling (Other) / photoreceptor (Other)
                      / retina (Other)},
      cin          = {AG Karl},
      ddc          = {610},
      cid          = {I:(DE-2719)1710004},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37213216},
      pmc          = {pmc:PMC10196395},
      doi          = {10.3389/fncel.2023.1106287},
      url          = {https://pub.dzne.de/record/258099},
}