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@ARTICLE{Ma:285735,
      author       = {Ma, Yuhua and Bauer, Helen Friedericke and Bockmann,
                      Juergen and Schön, Michael and Boeckers, Tobias M and Lutz,
                      Anne-Kathrin},
      title        = {{S}hank3 related oligodendrocyte alterations in autism are
                      restored by {E}rk pathway inhibition.},
      journal      = {Molecular psychiatry},
      volume       = {31},
      number       = {4},
      issn         = {1359-4184},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2026-00292},
      pages        = {1880 - 1897},
      year         = {2026},
      abstract     = {White matter abnormalities are consistently observed in
                      Shank3-related autism spectrum disorders (ASD), yet the
                      mechanisms underlying oligodendrocyte dysfunction and
                      myelination deficits remain poorly characterized. Here, we
                      demonstrate that Shank3 deficiency disrupts oligodendrocyte
                      development by promoting oligodendrocyte precursor cell
                      (OPC) proliferation while impairing functional maturation
                      and myelination. Mechanistically, Shank3 deficiency induced
                      hyperactivation of the Erk signalling pathway, which
                      compromised oligodendrocyte maturation and contributes to
                      hypomyelination. Pharmacological inhibition of the Erk
                      pathway effectively restored oligodendrocyte maturation in
                      vitro, rescued myelination deficits in vivo, and partially
                      improved autism-related behaviors and motor function in
                      Shank3-deficient mice. Transcriptomic analyses furtherly
                      revealed dysregulation of Wnt signalling, particularly the
                      upregulation of Wnt5a, a key ligand of the non-canonical Wnt
                      pathway, in Shank3-deficient oligodendrocytes. Consistently,
                      Wnt5a treatment was found to activate Erk signalling in
                      primary oligodendrocytes and replicate the observed
                      myelination deficits. These findings uncover the Wnt5a-Erk
                      axis as a critical regulator of oligodendrocyte dysfunction
                      in Shank3-related ASD and highlight its therapeutic
                      potential for addressing associated white matter deficits.},
      keywords     = {Animals / Male / Mice / Autistic Disorder: genetics /
                      Autistic Disorder: metabolism / Autistic Disorder:
                      physiopathology / Corpus Callosum: metabolism / Corpus
                      Callosum: physiopathology / MAP Kinase Signaling System /
                      Mice, Knockout / Molecular Targeted Therapy / Myelin Sheath:
                      genetics / Myelin Sheath: metabolism / Oligodendroglia:
                      physiology / Primary Cell Culture / White Matter: metabolism
                      / White Matter: physiopathology / Microfilament Proteins:
                      deficiency / Microfilament Proteins: genetics / Nerve Tissue
                      Proteins: deficiency / Nerve Tissue Proteins: genetics /
                      Shank3 protein, mouse (NLM Chemicals) / Microfilament
                      Proteins (NLM Chemicals) / Nerve Tissue Proteins (NLM
                      Chemicals)},
      cin          = {AG Böckers},
      ddc          = {610},
      cid          = {I:(DE-2719)1910002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41203933},
      pmc          = {pmc:PMC12999492},
      doi          = {10.1038/s41380-025-03333-1},
      url          = {https://pub.dzne.de/record/285735},
}