ReviewFrontiers in neurology2023
Pathology of myelin oligodendrocyte glycoprotein antibody-associated disease: a comparison with multiple sclerosis and aquaporin 4 antibody-positive neuromyelitis optica spectrum disorders.
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 32 papers.
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Who cites it
32 citing papers in PubMed.
- Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS.Annals of clinical and translational neurology · 2026Article
- Diagnostic Utility of Novel and Established Spinal MRI Signs in AQP4-IgG-Seropositive NMOSD Myelitis.Neurology · 2026Article
- Identification of risk factors for relapse at initial onset in myelin oligodendrocyte glycoprotein antibody-associated optic neuritis using ophthalmic findings.Japanese journal of ophthalmology · 2026Article
- Recognition and management of acute relapse of multiple sclerosis, neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein antibody-associated disease.Cell death and differentiation · 2026Review
- The cascade to pathogenicity in autoantibody-mediated CNS diseases.Brain : a journal of neurology · 2026Review
- Quantitative MRI Uncovers Subtle Cortical Damage in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.Annals of clinical and translational neurology · 2026Article
- Diagnostic Value of the Kappa Free Light Chain Index to Distinguish MOGAD, NMOSD, and MS.Neurology · 2026Article
- Characteristic patterns of complement deposition in NMOSD, MOGAD, and MS.Acta neuropathologica · 2026Article
- A rare presentation of pediatric MOG-antibody-associated neuroretinitis: a case report.BMC neurology · 2026Article
- Age at onset distinguishes clinical features and relapse risk in autoimmune glial fibrillary acidic protein astrocytopathy.Frontiers in immunology · 2026Article
- Ofatumumab Treatment Used in Pediatric MOGAD: A Retrospective Case Series.Journal of central nervous system disease · 2026Article
- Distinct macular structural and microvascular alterations differentiate neuromyelitis optica spectrum disorder from myelin oligodendrocyte glycoprotein antibody-associated disease in optic neuritis.Frontiers in immunology · 2026Article
- The relationship between serum MOG-IgG titer status and titers and the prognosis of pediatric MOGAD: a retrospective cohort study.Frontiers in pediatrics · 2026Article
- Targeting Lifestyle in CNS Inflammatory Demyelinating Diseases: Insights from Diet and Exercise as Potential Disease Modifiers.Brain sciences · 2025Review
- Neurofilament light chain levels differentiate ischemic from inflammatory optic neuropathies.Multiple sclerosis and related disorders · 2025Article
- Multi-tracer PET and MR imaging visualize distinct metabolic and inflammatory profiles in the white matter of NMOSD and MOGAD.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Diversity, Functional Complexity, and Translational Potential of Glial Cells in the Central Nervous System.International journal of molecular sciences · 2025Review
- Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Pathophysiology, Clinical Patterns, and Therapeutic Challenges of Intractable and Severe Forms.International journal of molecular sciences · 2025Review
- Serum sEV miRNAs as Biomarkers in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.Molecular neurobiology · 2025Article
- Article
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4 authors.
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Abstract
Myelin oligodendrocyte glycoprotein (MOG) is expressed on the outermost layer of the myelin sheath in the central nervous system. Recently, the clinical concept of MOG antibody-associated disease (MOGAD) was established based on the results of human MOG-transfected cell-based assays which can detect conformation-sensitive antibodies against MOG. In this review, we summarized the pathological findings of MOGAD and discussed the issues that remain unresolved. MOGAD pathology is principally inflammatory demyelination without astrocyte destruction, characterized by perivenous demyelination previously reported in acute disseminated encephalomyelitis and by its fusion pattern localized in both the white and gray matter, but not by radially expanding confluent demyelination typically seen in multiple sclerosis (MS). Some of demyelinating lesions in MOGAD show severe loss of MOG staining compared with those of other myelin proteins, suggesting a MOG-targeted pathology in the disease. Perivascular cuffings mainly consist of macrophages and T cells with CD4-dominancy, which is also different from CD8+ T-cell-dominant inflammation in MS. Compared to aquaporin 4 (AQP4) antibody-positive neuromyelitis optica spectrum disorders (NMOSD), perivenous complement deposition is less common, but can be seen on myelinated fibers and on myelin degradation products within macrophages, resembling MS Pattern II pathology. Thus, the pathogenetic contribution of complements in MOGAD is still debatable. Together, these pathological features in MOGAD are clearly different from those of MS and AQP4 antibody-positive NMOSD, suggesting that MOGAD is an independent autoimmune demyelinating disease entity. Further research is needed to clarify the exact pathomechanisms of demyelination and how the pathophysiology relates to the clinical phenotype and symptoms leading to disability in MOGAD patients.
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