ArticleAnnals of neurology2026
A Distinct Immunological Signature in Late-Onset Myasthenia Gravis: Insights from an Exploratory Proteomics Study.
Article in Annals of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02110706 (B Cell Targeted Treatment In Myasthenia Gravis), which is not on this map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
B Cell Targeted Treatment In Myasthenia Gravis (BeatMG): A Phase II Trial of Rituximab In Myasthenia Gravis
Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Age and Treatment Efficacy in Myasthenia Gravis: A Systematic Review, Meta-Analysis, and Meta-Regression.European journal of neurology · 2026Pooled it
- Half a century of change: demographic trends and their clinical impact in acetylcholine receptor antibody-positive myasthenia gravis.Journal of neurology · 2026Article
- AXIN1, STAMBP, ST1A1, CDCP1, and SIRT2 Validated as Myasthenia Gravis Biomarkers: A Comparative Proteomic Study With MS, CIDP, and Controls.European journal of neurology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
objectiveApproximately 80% of patients with myasthenia gravis (MG) have autoantibodies against acetylcholine receptor, and clinical characteristics may vary between early-onset (symptom onset age <50 years) and late-onset MG (EOMG and LOMG), but the pathophysiological differences between EOMG and LOMG are not well established.
methodsWe performed an exploratory in-depth proteomics analysis examining 768 inflammatory proteins utilizing the baseline serum samples from the BeatMG study (NCT02110706). We performed pathway enrichment analysis to assess the pathways involved in LOMG. A total of 15 selected proteins from the initial analysis were further examined using the UK Biobank and further quantified in a separate validation cohort.
resultsA total of 21 patients with EOMG (age 38.3 ± 12.1 years, 16 women [76.2%]) and 28 patients with LOMG (age 67.3 ± 8.6 years, 7 women [25%]) from the BeatMG study were included in the exploratory analysis. Several proteins involved in the regulation of leukocyte differentiation and myeloid leukocyte differentiation and migration pathways were more abundant in the LOMG group. Among them, 7 were significantly different in the UK Biobank cohort. A total of 80 participants (39 MG patients (age 54.33 ± 18.9 years, 17 women [43.6%]) and 41 healthy controls (age 49.56 ± 17.06 years, 21 women [66.1%]) were included in the validation cohort, and IL18R1, CXCL17, and CCL11 were validated to be specific for LOMG.
interpretationGrowing evidence supports that LOMG has a distinct immune pathomechanism. Further prospective studies are warranted to confirm the utility of these proteins as biomarkers of LOMG, and the feasibility of using them for more precise therapeutic targets to improve patient outcomes. ANN NEUROL 2026;99:198-210.
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