Clinical and Experimental Neuroimmunology最新文献

{"title":"Concurrent Hashimoto Encephalopathy and Papillary Thyroid Carcinoma: Separate Diagnostic Pathways, Shared Clinical Vigilance","authors":"Yun-Han Yang, Lien-Chung Wei","doi":"10.1111/cen3.70076","DOIUrl":"https://doi.org/10.1111/cen3.70076","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148752764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Safety and Effectiveness of Dimethyl Fumarate in Japanese Patients With Multiple Sclerosis: Subgroup Analysis of Older Patients and Patients Switching From Fingolimod or Natalizumab Using 2-Year Post-Marketing Surveillance Data","authors":"Ichiro Nakashima,&nbsp;Toshiyuki Fukazawa,&nbsp;Kazumasa Yokoyama,&nbsp;Takashi Yamamura,&nbsp;Hirofumi Ochi,&nbsp;Michihiro Kanda,&nbsp;Yayoi Sato,&nbsp;Ryusuke Sato,&nbsp;Haruki Makioka,&nbsp;Aya Tsuchiya,&nbsp;Takahiko Saida","doi":"10.1111/cen3.70074","DOIUrl":"https://doi.org/10.1111/cen3.70074","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>To evaluate the safety and effectiveness of dimethyl fumarate (DMF) in Japanese patients with multiple sclerosis (MS) in subgroups defined by baseline age and prior therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This analysis used 2-year post-marketing surveillance data from all MS patients receiving DMF in Japan between February 2017 and March 2024. Safety (adverse events, lymphocyte counts) and effectiveness (annualized relapse rate [ARR]) were assessed in patients aged &lt; 50, ≥ 50, &lt; 15, ≥ 15–&lt; 65, or ≥ 65 years at baseline, and in patients with no prior disease-modifying drug (DMD) therapy or switching from fingolimod or natalizumab.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Of 2092 patients, baseline age was &lt; 50 and ≥ 50 years in 1601 (76.5%) and 491 (23.5%) and &lt; 15, ≥ 15 to &lt; 65, and ≥ 65 years in 3 (0.1%), 2014 (96.3%), and 75 (3.6%), respectively; 576 (27.5%) had no prior DMD therapy, while 549 (26.2%), 71 (3.4%), and 896 (42.8%) had switched from fingolimod, natalizumab, and other DMDs, respectively. Lymphocyte count decreased occurred with higher incidence in the ≥ 65-year (34.7%) and prior fingolimod (40.6%) subgroups than the overall population (23.1%). Among relapsing–remitting MS patients (<i>n</i> = 1714), ARR significantly decreased at Years 1 and 2 after DMF initiation (−63.6% and −78.4% vs. the 1 year before DMF), with similar reductions in most age subgroups and in the no prior DMD subgroup. ARR non-significantly increased at Year 1 and decreased at Year 2 in the prior fingolimod or natalizumab subgroups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>DMF had consistent safety and effectiveness in Japanese MS patients, including older patients and those switching from fingolimod or natalizumab.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.70074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148752695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Safety and Effectiveness of Dimethyl Fumarate in Japanese Patients With Multiple Sclerosis: Subgroup Analysis of Older Patients and Patients Switching From Fingolimod or Natalizumab Using 2-Year Post-Marketing Surveillance Data","authors":"Ichiro Nakashima,&nbsp;Toshiyuki Fukazawa,&nbsp;Kazumasa Yokoyama,&nbsp;Takashi Yamamura,&nbsp;Hirofumi Ochi,&nbsp;Michihiro Kanda,&nbsp;Yayoi Sato,&nbsp;Ryusuke Sato,&nbsp;Haruki Makioka,&nbsp;Aya Tsuchiya,&nbsp;Takahiko Saida","doi":"10.1111/cen3.70074","DOIUrl":"https://doi.org/10.1111/cen3.70074","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>To evaluate the safety and effectiveness of dimethyl fumarate (DMF) in Japanese patients with multiple sclerosis (MS) in subgroups defined by baseline age and prior therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This analysis used 2-year post-marketing surveillance data from all MS patients receiving DMF in Japan between February 2017 and March 2024. Safety (adverse events, lymphocyte counts) and effectiveness (annualized relapse rate [ARR]) were assessed in patients aged &lt; 50, ≥ 50, &lt; 15, ≥ 15–&lt; 65, or ≥ 65 years at baseline, and in patients with no prior disease-modifying drug (DMD) therapy or switching from fingolimod or natalizumab.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Of 2092 patients, baseline age was &lt; 50 and ≥ 50 years in 1601 (76.5%) and 491 (23.5%) and &lt; 15, ≥ 15 to &lt; 65, and ≥ 65 years in 3 (0.1%), 2014 (96.3%), and 75 (3.6%), respectively; 576 (27.5%) had no prior DMD therapy, while 549 (26.2%), 71 (3.4%), and 896 (42.8%) had switched from fingolimod, natalizumab, and other DMDs, respectively. Lymphocyte count decreased occurred with higher incidence in the ≥ 65-year (34.7%) and prior fingolimod (40.6%) subgroups than the overall population (23.1%). Among relapsing–remitting MS patients (<i>n</i> = 1714), ARR significantly decreased at Years 1 and 2 after DMF initiation (−63.6% and −78.4% vs. the 1 year before DMF), with similar reductions in most age subgroups and in the no prior DMD subgroup. ARR non-significantly increased at Year 1 and decreased at Year 2 in the prior fingolimod or natalizumab subgroups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>DMF had consistent safety and effectiveness in Japanese MS patients, including older patients and those switching from fingolimod or natalizumab.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cen3.70074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148752694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-6 Blockade May Suppress the Alternative Complement Pathway in Neuromyelitis Optica Spectrum Disorders","authors":"Keishu Murakami,&nbsp;Yoshiaki Nakayama,&nbsp;Shoko Yorozu,&nbsp;Norimitsu Inoue,&nbsp;Katsuichi Miyamoto","doi":"10.1111/cen3.70075","DOIUrl":"https://doi.org/10.1111/cen3.70075","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Neuromyelitis optica spectrum disorders (NMOSDs) are complement-mediated autoimmune diseases of the central nervous system associated with anti-aquaporin-4 antibodies. While interleukin (IL)-6 signaling is implicated in NMOSD pathophysiology, its effects on the complement system remain unclear. We investigated the impact of IL-6 blockade on complement activation in NMOSD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We analyzed patients with NMOSD followed at our institution who had stored blood samples (serum and plasma) obtained during remission. Twenty-two patients during the remission phase were included: 12 treated with satralizumab (SAT) and 10 without biologics (Non-bio).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Levels of serum and plasma complement factors (Ba, factor H [FH], and sC5b-9) during the remission phase tended to be lower in the SAT group than in the Non-bio group, with a significant difference in serum Ba and plasma sC5b-9 and FH. Acute-phase serum Ba levels exceeded the reference range, indicating that the alternative pathway was activated during the acute phase and decreased during the remission phase. No relapses occurred after SAT therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>IL-6 is involved in complement production and activation through the induction of inflammation; therefore, IL-6 blockade may suppress complement production in patients with NMOSD and also inhibit activation of the alternative pathway. Our findings suggest a potential association between IL-6 inhibition and modulation of the alternative complement pathway in NMOSD, providing new insight into its therapeutic mechanism. Limitations include small sample size and limited plasma data.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148615500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-6 Blockade May Suppress the Alternative Complement Pathway in Neuromyelitis Optica Spectrum Disorders","authors":"Keishu Murakami,&nbsp;Yoshiaki Nakayama,&nbsp;Shoko Yorozu,&nbsp;Norimitsu Inoue,&nbsp;Katsuichi Miyamoto","doi":"10.1111/cen3.70075","DOIUrl":"https://doi.org/10.1111/cen3.70075","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Neuromyelitis optica spectrum disorders (NMOSDs) are complement-mediated autoimmune diseases of the central nervous system associated with anti-aquaporin-4 antibodies. While interleukin (IL)-6 signaling is implicated in NMOSD pathophysiology, its effects on the complement system remain unclear. We investigated the impact of IL-6 blockade on complement activation in NMOSD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We analyzed patients with NMOSD followed at our institution who had stored blood samples (serum and plasma) obtained during remission. Twenty-two patients during the remission phase were included: 12 treated with satralizumab (SAT) and 10 without biologics (Non-bio).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Levels of serum and plasma complement factors (Ba, factor H [FH], and sC5b-9) during the remission phase tended to be lower in the SAT group than in the Non-bio group, with a significant difference in serum Ba and plasma sC5b-9 and FH. Acute-phase serum Ba levels exceeded the reference range, indicating that the alternative pathway was activated during the acute phase and decreased during the remission phase. No relapses occurred after SAT therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>IL-6 is involved in complement production and activation through the induction of inflammation; therefore, IL-6 blockade may suppress complement production in patients with NMOSD and also inhibit activation of the alternative pathway. Our findings suggest a potential association between IL-6 inhibition and modulation of the alternative complement pathway in NMOSD, providing new insight into its therapeutic mechanism. Limitations include small sample size and limited plasma data.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148615530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological–Diagnostic Dissociation in Multiple Sclerosis: Early EBV-Associated Intrathecal Immune Activity","authors":"Okan Sokmen","doi":"10.1111/cen3.70073","DOIUrl":"https://doi.org/10.1111/cen3.70073","url":null,"abstract":"<p>EBV-associated intrathecal immune activity may precede radiological abnormalities and clinically recognizable multiple sclerosis. This biological–diagnostic dissociation supports the concept of a preclinical phase in MS evolution characterized by early compartmentalized CNS immune activation.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148386662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological–Diagnostic Dissociation in Multiple Sclerosis: Early EBV-Associated Intrathecal Immune Activity","authors":"Okan Sokmen","doi":"10.1111/cen3.70073","DOIUrl":"https://doi.org/10.1111/cen3.70073","url":null,"abstract":"<p>EBV-associated intrathecal immune activity may precede radiological abnormalities and clinically recognizable multiple sclerosis. This biological–diagnostic dissociation supports the concept of a preclinical phase in MS evolution characterized by early compartmentalized CNS immune activation.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148386707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Switching From Ravulizumab to Zilucoplan in Anti-Acetylcholine Receptor Antibody–Positive Generalized Myasthenia Gravis: A Case Report","authors":"Seiya Takahashi,&nbsp;Ryuta Kinno","doi":"10.1111/cen3.70072","DOIUrl":"https://doi.org/10.1111/cen3.70072","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Ravulizumab (RAV) is a long-acting complement C5 inhibitor used to treat anti-acetylcholine receptor (AChR)-positive generalized myasthenia gravis (gMG). However, fluctuations in symptoms have been observed in some patients during RAV therapy. Here, we describe a patient with anti-AChR antibody–positive gMG who developed recurrent worsening symptoms during the latter phase of the RAV dosing interval, and subsequently achieved symptom stabilization after switching to zilucoplan (ZIL).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>A 58-year-old man with anti-AChR antibody–positive gMG was treated with targeted immunotherapy and followed up longitudinally at our institution. He was diagnosed with gMG at 52 years of age and subsequently experienced repeated exacerbations and remissions. 6 years after disease onset, treatment with RAV was initiated, resulting in clinical improvement. However, after transitioning to the maintenance regimen, symptom recurrence consistently developed approximately 1 week before the next scheduled infusion. After switching to ZIL, these fluctuations resolved and his symptoms remained stable.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The clinical course of this patient suggests an association between RAV treatment and the periodic worsening of symptoms. In this patient, the symptoms stabilized after switching to ZIL in combination with ongoing immunotherapy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148386129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Switching From Ravulizumab to Zilucoplan in Anti-Acetylcholine Receptor Antibody–Positive Generalized Myasthenia Gravis: A Case Report","authors":"Seiya Takahashi,&nbsp;Ryuta Kinno","doi":"10.1111/cen3.70072","DOIUrl":"https://doi.org/10.1111/cen3.70072","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Ravulizumab (RAV) is a long-acting complement C5 inhibitor used to treat anti-acetylcholine receptor (AChR)-positive generalized myasthenia gravis (gMG). However, fluctuations in symptoms have been observed in some patients during RAV therapy. Here, we describe a patient with anti-AChR antibody–positive gMG who developed recurrent worsening symptoms during the latter phase of the RAV dosing interval, and subsequently achieved symptom stabilization after switching to zilucoplan (ZIL).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Case Presentation</h3>\u0000 \u0000 <p>A 58-year-old man with anti-AChR antibody–positive gMG was treated with targeted immunotherapy and followed up longitudinally at our institution. He was diagnosed with gMG at 52 years of age and subsequently experienced repeated exacerbations and remissions. 6 years after disease onset, treatment with RAV was initiated, resulting in clinical improvement. However, after transitioning to the maintenance regimen, symptom recurrence consistently developed approximately 1 week before the next scheduled infusion. After switching to ZIL, these fluctuations resolved and his symptoms remained stable.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The clinical course of this patient suggests an association between RAV treatment and the periodic worsening of symptoms. In this patient, the symptoms stabilized after switching to ZIL in combination with ongoing immunotherapy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148386329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Author's Reply to “Autoimmune Cerebellar Ataxia During TNF-α Inhibitor Therapy: Causality or Coincidence?”","authors":"Tomohide Ando,&nbsp;Nobuaki Yoshikura,&nbsp;Akira Takekoshi,&nbsp;Akio Kimura,&nbsp;Takayoshi Shimohata","doi":"10.1111/cen3.70071","DOIUrl":"https://doi.org/10.1111/cen3.70071","url":null,"abstract":"","PeriodicalId":10193,"journal":{"name":"Clinical and Experimental Neuroimmunology","volume":"17 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148324578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}