% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{OualiAlami:164314,
      author       = {Ouali Alami, Najwa and Tang, Linyun and Wiesner, Diana and
                      Commisso, Barbara and Bayer, David and Weishaupt, Jochen H
                      and Dupuis, Luc and Wong, Phillip and Baumann, Bernd and
                      Wirth, Thomas and Böckers, Tobias and Yilmazer-Hanke, Deniz
                      and Ludolph, Albert and Roselli, Francesco},
      title        = {{M}ultiplexed chemogenetics in astrocytes and motoneurons
                      restore blood–spinal cord barrier in {ALS}},
      journal      = {Life science alliance},
      volume       = {3},
      number       = {11},
      issn         = {2575-1077},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DZNE-2022-00968},
      pages        = {e201900571},
      year         = {2020},
      abstract     = {Blood-spinal cord barrier (BSCB) disruption is thought to
                      contribute to motoneuron (MN) loss in amyotrophic lateral
                      sclerosis (ALS). It is currently unclear whether impairment
                      of the BSCB is the cause or consequence of MN dysfunction
                      and whether its restoration may be directly beneficial. We
                      revealed that SOD1 G93A , FUS ΔNLS , TDP43 G298S , and Tbk1
                      +/- ALS mouse models commonly shared alterations in the
                      BSCB, unrelated to motoneuron loss. We exploit PSAM/PSEM
                      chemogenetics in SOD1 G93A mice to demonstrate that the BSCB
                      is rescued by increased MN firing, whereas inactivation
                      worsens it. Moreover, we use DREADD chemogenetics, alone or
                      in multiplexed form, to show that activation of Gi signaling
                      in astrocytes restores BSCB integrity, independently of MN
                      firing, with no effect on MN disease markers and
                      dissociating them from BSCB disruption. We show that
                      astrocytic levels of the BSCB stabilizers Wnt7a and Wnt5a
                      are decreased in SOD1 G93A mice and strongly enhanced by Gi
                      signaling, although further decreased by MN inactivation.
                      Thus, we demonstrate that BSCB impairment follows MN
                      dysfunction in ALS pathogenesis but can be reversed by
                      Gi-induced expression of astrocytic Wnt5a/7a.},
      keywords     = {Amyotrophic Lateral Sclerosis: blood / Amyotrophic Lateral
                      Sclerosis: metabolism / Animals / Astrocytes: metabolism /
                      Astrocytes: physiology / Disease Models, Animal / Disease
                      Progression / Female / Humans / Male / Mice / Mice, Inbred
                      C57BL / Mice, Transgenic / Motor Neurons: metabolism / Motor
                      Neurons: physiology / Spinal Cord: metabolism / Spine: blood
                      supply / Spine: metabolism / Superoxide Dismutase:
                      metabolism / Superoxide Dismutase-1: genetics / Superoxide
                      Dismutase-1: metabolism / Wnt Proteins: metabolism / Wnt-5a
                      Protein: metabolism},
      cin          = {AG Roselli / AG Böckers / Clinical Study Center Ulm},
      ddc          = {570},
      cid          = {I:(DE-2719)1910001 / I:(DE-2719)1910002 /
                      I:(DE-2719)5000077},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC7479971},
      pubmed       = {pmid:32900826},
      doi          = {10.26508/lsa.201900571},
      url          = {https://pub.dzne.de/record/164314},
}