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Quantitative Contribution of Clinical Attacks to Residual Disability in Patients With AQP4-Antibody Neuromyelitis Optica Spectrum Disorder.

Neurology

January 2025

From the Nuffield Department of Clinical Neurosciences (B.C., A.F., R.G., M.I.S.L., J.P.), Oxford University Hospitals, United Kingdom; Department of Neurology (B.C.), Tongji Hospital of Tongji Medical College, Huazhong University of Science of Technology, Wuhan, China; University Hospitals Sussex National Health Service Foundation Trust (S.A.C.), Brighton; Centre for Preventive Neurology (R.D.), Wolfson Institute of Population Health, Queen Mary University of London; Queen Square Multiple Sclerosis Centre (Y.H.), UCL Institute of Neurology, Faculty of Brain Sciences, University College London; Department of Paediatric Neurology (Y.H.), Great Ormond Street Hospital for Children, London; Department of Neurology (C. Halfpenny), University Hospital Southampton NHS Foundation Trust; Department of Neurology (C. Hemingway), Great Ormond Street Hospital for Children, London and Institute of Neurology; Department of Neurology (J.C.H.), University of Plymouth Faculty of Health and University Hospitals; Department of Ophthalmology (E.O.S.), King's College Hospital NHS Foundation Trust, London; Department of Neurology (W.R.), St George's University Hospitals NHS Foundation Trust, London; Department of Neurology (R.J.M.), Gloucestershire Hospitals National Health Service Foundation Trust; Department of Neurology (V.W.), King's College Hospital NHS Foundation Trust, London; Department of Neurology (V.W.), Guy's and St Thomas' National Health Service Foundation Trust, London; Department of Paediatric Neurology (S.R.), John Radcliffe Hospital, Oxford; and Neurology Department (R.G.), Wexham Park Hospital, Frimley Foundation Health Trust, Slough, United Kingdom.

Article Synopsis
  • The study investigates how clinical attacks contribute to ongoing disability in patients with aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD).
  • A total of 165 patients were analyzed using disability scores recorded after at least six months post-attack, with findings showing a significant increase in disability scores correlating with the number and type of relapses.
  • Results indicated that specific relapse types, particularly the combination of transverse myelitis and optic neuritis, had the most substantial impact on increasing residual disability.
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Article Synopsis
  • * Out of 250 cases, NMOSD had a higher rate of autoantibody positivity (25.5%) compared to MOGAD (12.2%), and double antibody positivity was also more common in NMOSD (5.9% vs. 1.4%).
  • * The study found that NMOSD patients with positive autoant
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Article Synopsis
  • - Autoimmune encephalitis (AIE) is a rare neurological disorder characterized by brain inflammation, often linked to specific autoantibodies; currently, there are no approved treatments for AIE despite the involvement of interleukin-6 (IL-6) signaling in its pathology.
  • - The CIELO study aims to test the efficacy and safety of satralizumab, an IL-6 receptor-targeting monoclonal antibody, in patients with specific types of AIE, using a randomized, double-blind design with 152 participants.
  • - The study will follow a 52-week treatment period with possible extensions, enabling participants to receive either the study drug, placebo, or additional treatment options depending on the
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Background: Aquaporin-4 (AQP4) antibody-associated neuromyelitis optica spectrum disorder (NMOSD) is an antibody-mediated inflammatory disease of the central nervous system. We have undertaken a systematic review and meta-analysis to ascertain the sex ratio and mean age of onset for AQP4 antibody associated NMOSD. We have also explored factors that impact on these demographic data.

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Serum Proteomics Distinguish Subtypes of NMO Spectrum Disorder and MOG Antibody-Associated Disease and Highlight Effects of B-Cell Depletion.

Neurol Neuroimmunol Neuroinflamm

July 2024

From the Arthritis and Clinical Immunology Research Program (S.G., G.K., R.M.K., K.M., J.M.G., Y.M.-D., G.P., R.C.A.), Oklahoma Medical Research Foundation; Department of Microbiology and Immunology (S.G., R.C.A.), Oklahoma University Health Science Center; NeuroCure Clinical Research Center and Experimental and Clinical Research Center (N.S., K.R., P.S., M.H., F.P.), Max Delbrueck Center for Molecular Medicine and Charité Universitätsmedizin Berlin; and Department of Neurology (N.S., K.R., P.S., M.H., F.P.), Charité Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany.

Background And Objectives: AQP4 antibody-positive NMOSD (AQP4-NMOSD), MOG antibody-associated disease (MOGAD), and seronegative NMOSD (SN-NMOSD) are neuroautoimmune conditions that have overlapping clinical manifestations. Yet, important differences exist in these diseases, particularly in B-cell depletion (BCD) efficacy. Yet, the biology driving these differences remains unclear.

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