ArticleActa neuropathologica2020
The pathology of central nervous system inflammatory demyelinating disease accompanying myelin oligodendrocyte glycoprotein autoantibody.
Article in Acta neuropathologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 3 of them syntheses 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
194 citing papers in PubMed, 3 syntheses or guidelines pooled it, 351 citations in OpenAlex.
- Biomarkers to predict relapse in myelin oligodendrocyte glycoprotein antibody-associated disease: a systematic review and meta-analysis.Journal of neurology, neurosurgery, and psychiatry · 2026Pooled it
- Clinical features and management of coexisting anti-N-methyl-D-aspartate receptor encephalitis and myelin oligodendrocyte glycoprotein antibody-associated encephalomyelitis: a case report and review of the literature.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Pooled it
- Imaging cortical multiple sclerosis lesions with ultra-high field MRI.NeuroImage. Clinical · 2021Pooled it
- Use of MRI in neuromyelitis optica spectrum disorder and myelin oligodendrocyte glycoprotein antibody-associated disease - MAGNIMS consensus recommendations.Nature reviews. Neurology · 2026Review
- Review
- Role of complement and complement-targeted therapeutics in neurological diseases.Nature reviews. Neurology · 2026Review
- Use of Fluid Biomarkers in NMOSD and MOGAD: Clinical and Research Applications.Neurology(R) neuroimmunology & neuroinflammation · 2026Review
- Psychiatric comorbidities cluster early after onset in MOGAD: a cross-sectional comparative study with MS and NMOSD.Journal of neurology, neurosurgery, and psychiatry · 2026Article
- Quantitative MRI Uncovers Subtle Cortical Damage in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.Annals of clinical and translational neurology · 2026Article
- Myelin Oligodendrocyte Glycoprotein Antibody-Associated Cerebral Cortical Encephalitis: A Comparative Study With Antibody-Negative and Non-MOG Antibody-Positive Cortical Encephalitis in Chinese Adults.CNS neuroscience & therapeutics · 2026Article
- Demyelinating disorders in women: epidemiology, immunology, and clinical implications across MS, NMOSD, and MOGAD.Journal of neurology · 2026Review
- Serum and CSF cytokine profile impact clinical phenotype in pediatric MOGAD.Journal of neuroinflammation · 2026Article
- Granulocyte and astrocyte markers distinguish MOG-antibody disease and neuromyelitis optica from multiple sclerosis.Brain : a journal of neurology · 2026Observational
- Complement C4d Informs the Differential Diagnosis of Inflammatory Demyelinating CNS Diseases.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Role of serum complement C3 in blood-brain barrier injury and prognosis of anti-NMDAR encephalitis.BMC neurology · 2026Article
- Investigating the Frequency and Outcome of Central Vein Sign and Paramagnetic Rim Lesions in Children With MOGAD.Neurology · 2026Article
- Characteristic patterns of complement deposition in NMOSD, MOGAD, and MS.Acta neuropathologica · 2026Article
- From the Optic Neuritis Treatment Trial to Antibody-Mediated Optic Neuritis: Four Decades of Progress and Unanswered Questions.Biomedicines · 2026Review
- Expanding Evidence of Leptomeningeal Involvement in MOGAD and Its Relevance to Its Pathophysiology.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- Biomarkers for myelin oligodendrocyte glycoprotein-associated disease: recent advances and future.Frontiers in immunology · 2026Review
134 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
We sought to define the pathological features of myelin oligodendrocyte glycoprotein (MOG) antibody associated disorders (MOGAD) in an archival autopsy/biopsy cohort. We histopathologically analyzed 2 autopsies and 22 brain biopsies from patients with CNS inflammatory demyelinating diseases seropositive for MOG-antibody by live-cell-based-assay with full length MOG in its conformational form. MOGAD autopsies (ages 52 and 67) demonstrate the full spectrum of histopathological features observed within the 22 brain biopsies (median age, 10 years; range, 1-66; 56% female). Clinical, radiologic, and laboratory characteristics and course (78% relapsing) are consistent with MOGAD. MOGAD pathology is dominated by coexistence of both perivenous and confluent white matter demyelination, with an over-representation of intracortical demyelinated lesions compared to typical MS. Radially expanding confluent slowly expanding smoldering lesions in the white matter as seen in MS, are not present. A CD4+ T-cell dominated inflammatory reaction with granulocytic infiltration predominates. Complement deposition is present in all active white matter lesions, but a preferential loss of MOG is not observed. AQP4 is preserved, with absence of dystrophic astrocytes, and variable oligodendrocyte and axonal destruction. MOGAD is pathologically distinguished from AQP4-IgG seropositive NMOSD, but shares some overlapping features with both MS and ADEM, suggesting a transitional pathology. Complement deposition in the absence of selective MOG protein loss suggest humoral mechanisms are involved, however argue against endocytic internalization of the MOG antigen. Parallels with MOG-EAE suggest MOG may be an amplification factor that augments CNS demyelination, possibly via complement mediated destruction of myelin or ADCC phagocytosis.
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What Socratic holds
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.