Evidence map›Paper›PMID 40155000›Full record

ArticleJournal of neurology, neurosurgery, and psychiatry2025

MOG antibody non-P42 epitope is associated with a higher risk of relapse in paediatric MOGAD.

Aseel El Hajj, Anne Ruiz, Antoine Gavoille, Justine Couturier, Pascale Giraudon, Lakhdar Benyahya, Lisa Malaise, Maxime Bigotte, Claire Benetollo, Gaetan Amorim and 10 more

Abstract read
In one paragraph

Article in Journal of neurology, neurosurgery, and psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors.

Aseel El HajjForgetting Team, CNRS, INSERM, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292, Université Claude Bernard Lyon 1, Lyon, France.
Anne RuizCNRS, INSERM, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292, Université Claude Bernard Lyon 1, Bron, France.
Antoine GavoilleService de neurologie, sclérose en plaques, pathologies de la myéline et neuroinflammation and Centre de référence des maladies inflammatoires rares du cerveau et de la moelle (MIRCEM), Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon, Lyon, France.
Justine CouturierCNRS, INSERM, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292, Université Claude Bernard Lyon 1, Bron, France.
Pascale GiraudonCNRS, INSERM, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292, Université Claude Bernard Lyon 1, Bron, France.
Lakhdar BenyahyaCentre de Référence des Maladies Inflammatoires Rares du Cerveau et de la Moelle, Hospices Civils de Lyon, Lyon, France.
Lisa MalaiseCNRS, INSERM, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292, Université Claude Bernard Lyon 1, Bron, France.
Maxime BigotteCNRS, INSERM, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292, Université Claude Bernard Lyon 1, Bron, France.
Claire BenetolloCNRS, INSERM, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292, Université Claude Bernard Lyon 1, Bron, France.
Gaetan AmorimCNRS, INSERM, Centre de Recherche en Neurosciences de Lyon CRNL U1028 UMR5292, Université Claude Bernard Lyon 1, Bron, France.
Julia RouxDepartment of Pediatric Neurology, Bicêtre Hospital, Le Kremlin Bicêtre, France.
Carole LeroyUMR 1184-CEA-IDMIT, Center for Immunology of Viral Infections and Autoimmune Diseases, Université Paris-Sud Faculté de Médecine, Le Kremlin-Bicetre, France.
Ann-Kathrin KogelKatholisches Klinikum Bochum Sankt Josef-Hospital, Bochum, Germany.ORCID http://orcid.org/0000-0002-8217-6063
Ilya AyzenbergDepartment of Neurology, Katholisches Klinikum Bochum Sankt Josef-Hospital, Bochum, Germany.
Friedemann PaulNeuroCure Clinical Research Center, Charité, Berlin, Germany.
Sudarshini RamanathanTranslational Neuroimmunology Group, Sydney Medical School, Faculty of Medicine and Health, University of Sydney, Sydney, New South Wales, Australia.ORCID http://orcid.org/0000-0002-0294-9768
Russell C DaleNeuroimmunology Group, Institute for Neuroscience and Muscle Research, Kids Research Institute at the Children's Hospital, University of Sydney, Sydney, New South Wales, Australia.ORCID http://orcid.org/0000-0002-2495-1826
Kumaran DeivaPaediatric Neurology, Assistance Publique-Hôpitaux de Paris, Hôpital Bicêtre,National Referral Centre for Neuro-Inflammatory Diseases in Children, Le Kremlin Bicêtre, France.
Fabienne BrilotBrain Autoimmunity, Kids Neuroscience Centre, Kids Research at the Children's Hospital, Sydney, New South Wales, Australia.ORCID http://orcid.org/0000-0002-7025-2276
Romain MarignierService de Neuro-Inflammation, Hopital Neurologique et Neurochirurgical Pierre Wertheimer, Lyon, France marignierro@gmail.com.ORCID http://orcid.org/0000-0002-5967-2800

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBiomarkers for predicting myelin oligodendrocyte glycoprotein antibody (Ab)-associated disease (MOGAD) clinical course are still missing. Binding capacity to a mutant MOG protein variant (MOG-P42S; non-P42) was shown to correlate with an increased relapse risk in adult patients.The objective of our study was to assess the frequency of binding to the non-P42 MOG variant in a cohort of paediatric MOGAD and to investigate its association with specific clinical profiles and disease course.

methodsWe included children with MOG-Ab seropositive samples collected after their first demyelinating episode from five different centres. We performed live cell-based assays with native full-length MOG (MOG-FL) and mutant MOG-P42S and correlated the results with clinical data.

resultsOf the 81 MOG-FL identified patients serum, 40 bound the non-P42 MOG. Non-P42 patients exhibited an earlier median age of onset (p=0.002). Phenotype distribution was different between groups (p=0.001), with non-P42 patients predominantly exhibiting acute disseminated encephalomyelitis phenotype. Notably, the non-P42 group was associated with a higher relapse rate (relative rate: 2.6 (95% CI 1.1 to 6.2), p=0.03), adjusted for clinical phenotype.

conclusionNon-P42 is a promising biomarker for predicting relapse in paediatric MOGAD patients.

Indexed as

AutoantibodiesEpitopesMyelin-Oligodendrocyte GlycoproteinMyelin Oligodendrocyte Glycoprotein Antibody-Associated DiseaseAdolescentBiomarkersChildChild, PreschoolFemaleHumansMaleRecurrenceAutoantibodiesBiomarkersEpitopesMOG protein, humanMyelin-Oligodendrocyte GlycoproteinNEUROIMMUNOLOGY

Identifiers

PMID40155000
PMCPMC12322422

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.