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@ARTICLE{Stascheit:283152,
      author       = {Stascheit, Frauke and Preßler, Hannah and Stein, Kerstin
                      and Pernice, Helena Franziska and Hahn, Katrin and Meisel,
                      Andreas and Lünemann, Jan D},
      title        = {{A}berrant {C}omplement {A}ctivation {I}s a {P}rominent
                      {F}eature of {C}hronic {I}nflammatory {D}emyelinating
                      {P}olyneuropathy.},
      journal      = {Neurology: Neuroimmunology $\&$ Neuroinflammation ;
                      official journal of the American Academy of Neurology},
      volume       = {13},
      number       = {2},
      issn         = {2332-7812},
      address      = {Philadelphia, Pa.},
      publisher    = {Wolters Kluwer},
      reportid     = {DZNE-2026-00048},
      pages        = {e200542},
      year         = {2026},
      abstract     = {To comprehensively characterize complement pathway
                      activation in chronic inflammatory demyelinating
                      polyneuropathy (CIDP) and its association with clinical
                      disease features using advanced complement
                      profiling.Complement protein levels indicative of classical,
                      lectin, and alternative pathway activation were quantified
                      by multiplex ELISA and compared between 28 patients with
                      typical CIDP, 24 patients with Charcot-Marie Tooth
                      neuropathy (CMT), and 24 demographically matched healthy
                      controls (HD).Serum levels of activated complement
                      proteins-C3a, C4a, Ba, Bb, C5a, and the soluble terminal
                      complement complex sC5b-9 (sTCC)-were significantly elevated
                      in CIDP patients compared to healthy donors (HD) (p <
                      0.001). Except for C3a, these protein levels were also
                      significantly higher in CIDP patients than in those with
                      Charcot-Marie-Tooth disease (CMT). Among CIDP patients,
                      those with active, unstable disease exhibited significantly
                      higher levels of terminal complement components (C5a and
                      sTCC) compared to patients with stable disease or in
                      remission (p < 0.001).These findings highlight the critical
                      involvement of aberrant complement activation in the
                      pathophysiology of CIDP and provide a rationale for further
                      investigation into targeted complement inhibition as a
                      therapeutic approach.},
      keywords     = {Humans / Polyradiculoneuropathy, Chronic Inflammatory
                      Demyelinating: blood / Polyradiculoneuropathy, Chronic
                      Inflammatory Demyelinating: immunology /
                      Polyradiculoneuropathy, Chronic Inflammatory Demyelinating:
                      physiopathology / Male / Female / Middle Aged / Complement
                      Activation: physiology / Adult / Charcot-Marie-Tooth
                      Disease: blood / Charcot-Marie-Tooth Disease: immunology /
                      Aged},
      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:41499725},
      doi          = {10.1212/NXI.0000000000200542},
      url          = {https://pub.dzne.de/record/283152},
}