ReviewFrontiers in neurology2023
Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease.
Review in Frontiers in neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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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.
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Who cites it
61 citing papers in PubMed, 85 citations in OpenAlex.
- Current Applications of Artificial Intelligence in Neuro-Ophthalmic Imaging: A Narrative Approach.Medical sciences (Basel, Switzerland) · 2026Review
- Modeling pathogenic B cell function in experimental autoimmune encephalomyelitis.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Article
- Recurrent Myelin Oligodendrocyte Glycoprotein Antibody-Positive Aseptic Meningitis at the Identical Site in a Child: Leptomeningeal Enhancement Detected by Contrast-Enhanced FLAIR Imaging.Yonago acta medica · 2026Article
- Demyelinating disorders in women: epidemiology, immunology, and clinical implications across MS, NMOSD, and MOGAD.Journal of neurology · 2026Review
- Functional and structural outcomes in paediatric myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): a prospective study.Documenta ophthalmologica. Advances in ophthalmology · 2026Article
- Novel CSF biomarkers for facilitating diagnosis of CNS-HLH from other neuroinflammatory disorders.Blood advances · 2026Article
- A rare presentation of pediatric MOG-antibody-associated neuroretinitis: a case report.BMC neurology · 2026Article
- Article
- CAR T-Cell Immunotherapy in Neuroautoimmune Diseases: Focus on the Central Nervous System.Biomedicines · 2026Review
- Cognitive function in patients with myelin oligodendrocyte glycoprotein antibody-associated disease.Journal of neurology · 2026Article
- Biomarkers for myelin oligodendrocyte glycoprotein-associated disease: recent advances and future.Frontiers in immunology · 2026Review
- MOG-Ab-associated optic neuritis with concurrent GFAP-Ab positivity following tislelizumab-based treatment: a case report.Frontiers in pharmacology · 2026Article
- The emerging role of B cells in immune-mediated demyelinating diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Eosinophil Recruitment and Activity in CNS Lesions of MOG Antibody-Associated Myelitis Following Influenza Vaccination: A Case Report.Case reports in neurological medicine · 2026Article
- Clinical and laboratory findings in patients with anti-myelin oligodendrocyte glycoprotein antibodies: experience from two tertiary hospitals in Madrid.Frontiers in immunology · 2026Article
- Bruton Tyrosine Kinase Inhibition Limits Multiple Sclerosis Disease-Driving Inflammation While Promoting Regulatory B Cells.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- MOG IgG3-Subclass Antibodies in MOG-Associated Disease: Insights From a Pediatric Case With IgG1 Deficiency and Literature Review.Neurology(R) neuroimmunology & neuroinflammation · 2026Review
- A-to-I RNA editing profiles and distinct immune responses in myelin oligodendrocyte glycoprotein antibody-positive optic neuritis.Frontiers in immunology · 2026Article
- Stem cell-derived extracellular vesicles as immunomodulatory agents: targeting pathological crosstalk in systemic lupus erythematosus and multiple sclerosis.Frontiers in medicine · 2026Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) is a spectrum of diseases, including optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, and cerebral cortical encephalitis. In addition to distinct clinical, radiological, and immunological features, the infectious prodrome is more commonly reported in MOGAD (37-70%) than NMOSD (15-35%). Interestingly, pediatric MOGAD is not more aggressive than adult-onset MOGAD, unlike in multiple sclerosis (MS), where annualized relapse rates are three times higher in pediatric-onset MS. MOGAD pathophysiology is driven by acute attacks during which T cells and MOG antibodies cross blood brain barrier (BBB). MOGAD lesions show a perivenous confluent pattern around the small veins, lacking the radiological central vein sign. Initial activation of T cells in the periphery is followed by reactivation in the subarachnoid/perivascular spaces by MOG-laden antigen-presenting cells and inflammatory CSF milieu, which enables T cells to infiltrate CNS parenchyma. CD4+ T cells, unlike CD8+ T cells in MS, are the dominant T cell type found in lesion histology. Granulocytes, macrophages/microglia, and activated complement are also found in the lesions, which could contribute to demyelination during acute relapses. MOG antibodies potentially contribute to pathology by opsonizing MOG, complement activation, and antibody-dependent cellular cytotoxicity. Stimulation of peripheral MOG-specific B cells through TLR stimulation or T follicular helper cells might help differentiate MOG antibody-producing plasma cells in the peripheral blood. Neuroinflammatory biomarkers (such as MBP, sNFL, GFAP, Tau) in MOGAD support that most axonal damage happens in the initial attack, whereas relapses are associated with increased myelin damage.
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Registered trials
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 Socratic graph.