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@ARTICLE{Weiser:280248,
      author       = {Weiser, Judith and Rau, Alexander and von Zedtwitz,
                      Katharina and Feige, Bernd and Nickel, Kathrin and Maier,
                      Simon J and Dressle, Raphael J and Venhoff, Nils and van
                      Elst, Ludger Tebartz and Schiele, Miriam A and Domschke,
                      Katharina and Prüss, Harald and Endres, Dominique},
      title        = {{S}ocial anxiety disorder and antibodies against glial
                      cells in the cerebrospinal fluid.},
      journal      = {Brain, behavior, $\&$ immunity - health},
      volume       = {48},
      issn         = {2666-3546},
      address      = {[Amsterdam]},
      publisher    = {Elsevier B.V.},
      reportid     = {DZNE-2025-00926},
      pages        = {101064},
      year         = {2025},
      abstract     = {Autoimmune social anxiety disorders have not yet been
                      described in the literature.Therefore, this case of a
                      patient with possible autoimmune-mediated social anxiety
                      disorder is presented. Due to treatment resistance and high
                      serum streptococcal antibody levels, a comprehensive
                      diagnostic work-up was performed.The 19-year-old female
                      patient presented with predominant social anxiety disorder
                      and secondary depression. Testing for all known
                      characterized neuronal and glial IgG antibodies identified
                      slightly positive ('+') recoverin IgG antibodies only in the
                      serum (using an immunoassay). Cerebrospinal fluid (CSF)
                      analysis using a tissue-based assay on unfixed mouse brain
                      slices revealed moderate immunoglobulin G (IgG) anti-nuclear
                      binding and a specific strong IgG binding against cell
                      nuclei of the Bergmann glia in the cerebellum. No clear
                      pathology was noted in conventional magnetic resonance
                      imaging (MRI), voxel-based morphometry, and cerebral blood
                      flow. Diffusion microstructure imaging (DMI) revealed a
                      substantial reduction of the intraneurite volume fraction in
                      the cerebellar gray and white matter. This was accompanied
                      by a compensatory increase in free fluid and the
                      extra-neurite volume fraction. Alterations in the striatum
                      were also observed with DMI. Electroencephalography (EEG)
                      showed intermittent generalized slowing with underlying left
                      frontal, right temporal, and left temporo-occipital
                      components (detected via independent component analysis of
                      the EEG). The [18F]fluorodeoxyglucose positron emission
                      tomography of the whole body detected a slight polyserositis
                      and no malignant tumor.This is the first description of a
                      case with evidence of a possible antibody-mediated
                      cerebellar dysfunction associated with social anxiety
                      disorder. The testing for all characterized neuronal/glial
                      antibodies showed only weakly positive recoverin antibodies
                      in the serum, which, however, were not detectable in the
                      CSF. Therefore, novel CSF antibodies directed against cell
                      nuclei of the Bergmann glia in the cerebellum could be
                      assumed. DMI alterations in the cerebellum were in principle
                      compatible with neuroinflammation with edematization and
                      cellular activation. In addition, the further DMI
                      alterations in the striatum and the fronto-temporal
                      generators of EEG slowing suggest an involvement of the
                      'anxiety network'. Further immunopsychiatric research in
                      anxiety disorders might contribute to identifying an
                      autoimmune subtype and potentially immunomodulatory
                      treatment options.},
      keywords     = {Anxiety (Other) / Autoimmune (Other) / Inflammation (Other)
                      / Recoverin (Other) / Social phobia (Other)},
      cin          = {AG Prüß},
      ddc          = {610},
      cid          = {I:(DE-2719)1810003},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40746968},
      pmc          = {pmc:PMC12312059},
      doi          = {10.1016/j.bbih.2025.101064},
      url          = {https://pub.dzne.de/record/280248},
}