{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T01:22:21Z","timestamp":1788398541416,"version":"build-2803163510"},"reference-count":38,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T00:00:00Z","timestamp":1774310400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T00:00:00Z","timestamp":1774310400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100007129","name":"Natural Science Foundation of Shandong Province","doi-asserted-by":"publisher","award":["ZR2024MH292"],"award-info":[{"award-number":["ZR2024MH292"]}],"id":[{"id":"10.13039\/501100007129","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81771298"],"award-info":[{"award-number":["81771298"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Although immunoglobulin G (IgG) autoantibodies against gangliosides are well\u2010established in axonal Guillain\u2010Barr\u00e9 syndrome (GBS), specific autoantibodies in demyelinating GBS\u2014including acute inflammatory demyelinating polyneuropathy (AIDP) and its variant, bifacial weakness with paresthesias (BFP)\u2014remain unidentified. We aimed to identify novel autoantibodies and clarify the immunological link between AIDP and BFP.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Immunoprecipitation and mass spectrometry identified gelsolin from BFP serum IgG targeting non\u2010compact, periaxonal myelin surrounding the nodes of Ranvier. Western blotting confirmed specific recognition of gelsolin\u20103, with no cross\u2010reactivity to the other 2 isoforms. Anti\u2013gelsolin\u20103 IgG prevalence was screened in 388 GBS patients and correlated with clinical and electrophysiological phenotypes. In vivo pathogenicity was assessed by intraneural IgG injection.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Anti\u2013gelsolin\u20103 IgG antibodies were detected in 24 GBS patients (6%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001 vs both disease and healthy controls), with no positive controls. These autoantibodies were strongly associated with facial weakness (63% vs 18%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) and the AIDP electrophysiological classification (73% vs 31%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). In vivo, these IgG1 autoantibodies bound to the nodal regions, triggering complement\u2010dependent nodal injury, voltage\u2010gated sodium channel cluster disruption, and concomitant demyelination. These early pathogenic events preceded macrophage infiltration.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>Anti\u2013gelsolin\u20103 IgG1 represents a novel biomarker linking AIDP and BFP. Our results provide the first evidence that AIDP can be formally classified as a nodo\u2010paranodopathy. This IgG1\u2010mediated, complement\u2010dependent nodal injury establishes a unifying paradigm across GBS: nodal complement activation represents a shared mechanism underlying conduction block despite targeting distinct domains\u2014the axolemma in AMAN and myelin components at the axon\u2013myelin interface in AIDP. ANN NEUROL 2026;99:1486\u20131501<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.78198","type":"journal-article","created":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T04:20:57Z","timestamp":1774412457000},"page":"1486-1501","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Gelsolin\u20103: A Novel Myelin Autoantigen in Demyelinating Guillain\u2010Barr\u00e9 Syndrome"],"prefix":"10.1002","volume":"99","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3145-9362","authenticated-orcid":false,"given":"Yuzhong","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Neurology Affiliated Hospital of Jining Medical University  Jining China"},{"name":"Medical Research Center Affiliated Hospital of Jining Medical University  Jining China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaomin","family":"Gao","sequence":"additional","affiliation":[{"name":"Medical 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