ArticleJournal of neuroinflammation2022
CSF GFAP levels in double seronegative neuromyelitis optica spectrum disorder: no evidence of astrocyte damage.
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- The Role of Glial Fibrillary Acidic Protein as a Biomarker in Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorder: A Systematic Review and Meta-Analysis.Medicina (Kaunas, Lithuania) · 2024Pooled it
- Serum GFAP and Age Accurately Distinguish AQP4-IgG Positive and Double Seronegative NMOSD From MOGAD After a Recent Attack.European journal of neurology · 2026Article
- Use of Fluid Biomarkers in NMOSD and MOGAD: Clinical and Research Applications.Neurology(R) neuroimmunology & neuroinflammation · 2026Review
- miR-6836-5p Drives Astrocyte Pro-survival Signaling Through DLG2-Hippo-YAP Pathway Under AQP4-IgG + ve NMOSD Stress.Molecular neurobiology · 2026Article
- Granulocyte and astrocyte markers distinguish MOG-antibody disease and neuromyelitis optica from multiple sclerosis.Brain : a journal of neurology · 2026Observational
- Neuroglial markers of damage in autoimmune neurology.Therapeutic advances in neurological disorders · 2026Review
- Predict disabling severe attacks in neuromyelitis optica spectrum disorders: warning symptoms and innovative machine learning models.Journal of translational medicine · 2025Article
- Double-negative NMOSD: from case report to a proposed diagnostic and therapeutic algorithm.BMC neurology · 2025Article
- Progression independent of relapse activity and relapse-associated worsening in seronegative NMOSD: an international cohort study.Journal of neurology · 2025Article
- Clinical characteristics of double negative atypical inflammatory demyelinating disease: A prospective study.Annals of clinical and translational neurology · 2024Article
- Neuromyelitis Optica Spectrum Disorder Resembling Wernicke's Encephalopathy: A Case Report and Review of the Literature.The Neurohospitalist · 2024Article
- Serum Biomarker Profiles Discriminate AQP4 Seropositive and Double Seronegative Neuromyelitis Optica Spectrum Disorder.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- Clinical Usefulness of a Cell-based Assay for Detecting Myelin Oligodendrocyte Glycoprotein Antibodies in Central Nervous System Inflammatory Disorders.Annals of laboratory medicine · 2024Article
- Soluble biomarkers for Neuromyelitis Optica Spectrum Disorders: a mini review.Frontiers in neurology · 2024Review
- Double-negative neuromyelitis optica spectrum disorder.Multiple sclerosis (Houndmills, Basingstoke, England) · 2023Review
- Disease characteristics of idiopathic transverse myelitis with serum neuronal and astroglial damage biomarkers.Scientific reports · 2023Article
- Peripheral Blood Th1/Th17 Immune Cell Shift is Associated with Disease Activity and Severity of AQP4 Antibody Sero-Positive Neuromyelitis Optica Spectrum Disorder.Neuropsychiatric disease and treatment · 2023Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 5 countries.
Funding
Abstract
backgroundDespite rigorous confirmation with reliable assays, some individuals showing the neuromyelitis optica spectrum disorder (NMOSD) phenotype remain negative for both aquaporin-4 (AQP4) and myelin oligodendrocyte glycoprotein (MOG) antibodies.
objectiveWe aimed to investigate whether double seronegative NMOSD (DN-NMOSD) and NMOSD with AQP4 antibody (AQP4-NMOSD) share the same pathophysiological basis, astrocytopathy, by measurement of cerebrospinal fluid (CSF) glial fibrillary acidic protein (GFAP) levels as a marker of astrocyte damage.
methodsSeventeen participants who (1) satisfied the 2015 diagnostic criteria for NMOSD, and (2) tested negative for AQP4 and MOG antibodies confirmed with repeated cell-based assays, and (3) had available CSF samples obtained at the point of clinical attacks, were enrolled from 4 medical centers (South Korea, Germany, Thailand, and Denmark). Thirty age-matched participants with AQP4-NMOSD, 17 participants with MOG antibody associated disease (MOGAD), and 15 participants with other neurological disorders (OND) were included as controls. The concentration of CSF GFAP was measured using enzyme-linked immunosorbent assay.
resultsCSF GFAP levels in the DN-NMOSD group were significantly lower than those in the AQP4-NMOSD group (median: 0.49 versus 102.9 ng/mL; p < 0.001), but similar to those in the OND (0.25 ng/mL) and MOGAD (0.39 ng/mL) control groups. The majority (90% (27/30)) of participants in the AQP4-NMOSD group showed significantly higher CSF GFAP levels than the highest level measured in the OND group, while no participant in the DN-NMOSD and MOGAD groups did.
conclusionsThese results suggest that DN-NMOSD has a different underlying pathogenesis other than astrocytopathy, distinct from AQP4-NMOSD.
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