MOGAD

1. Disease Information

1.1 Overview (current understanding)

MOGAD is a rare, antibody-mediated inflammatory demyelinating disorder of the central nervous system (CNS) associated with serum (and sometimes CSF) MOG-IgG detected by cell-based assays, and is considered distinct from multiple sclerosis (MS) and aquaporin-4 (AQP4)-IgG neuromyelitis optica spectrum disorder (NMOSD). (voase2024diagnosticcriteriafor pages 1-2, alani2023myelinoligodendrocyteglycoprotein pages 3-4, jeyakumar2024mogantibodyassociatedoptic pages 1-2)

Direct abstract quote (definition/distinct entity): - Gklinos & Dobson (2024-05-xx) state: “Clinical syndromes associated with antibodies against myelin oligodendrocyte glycoprotein (MOG) are now recognized as a distinct neurological disease entity…” (Antibodies; https://doi.org/10.3390/antib13020043) (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3)

1.2 Key identifiers and terminologies

• Preferred name: Myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD). (alani2023myelinoligodendrocyteglycoprotein pages 3-4)
• Common synonyms: MOG antibody disease; MOG-IgG–associated disease; MOG-IgG–associated disorder(s); MOG encephalomyelitis (legacy terminology). (alani2023myelinoligodendrocyteglycoprotein pages 3-4, forcadela2024timingofmogigg pages 1-2)
• ICD/MeSH/Orphanet/OMIM codes: Not extractable from the retrieved evidence snippets in this run; a 2025 review notes existence of “unique international classification of diseases code (ICD-10-…)” but the code string was not present in accessible text. (NCT05271409 chunk 3)

1.3 Evidence provenance

Most knowledge summarized here is derived from aggregated disease-level resources (multi-center cohorts, registries, systematic reviews, consensus criteria, and clinical trial registries), not single-patient EHR-derived datasets. (alani2023myelinoligodendrocyteglycoprotein pages 3-4, forcadela2024timingofmogigg pages 1-2, varley2024validationofthe pages 1-2, NCT05063162 chunk 1, NCT05271409 chunk 1)

2. Etiology

2.1 Disease causal factors (mechanistic)

MOGAD is primarily an autoantibody-associated disease targeting MOG (a surface myelin/oligodendrocyte protein). Pathogenesis likely requires cooperation between humoral immunity (MOG-IgG) and cellular immune processes, as well as CNS barrier dysfunction permitting antibody/immune cell access. (abraham2024myelinoligodendrocyteantibody pages 10-13, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3, abraham2024myelinoligodendrocyteantibody pages 8-10)

2.2 Risk factors

Demographic risk context (not causal): disease occurs in both children and adults with a biphasic age distribution (see Epidemiology). (jeyakumar2024mogantibodyassociatedoptic pages 1-2)

Potential triggers (environment/infectious): initiating events proposed include infections leading to autoimmunity (molecular mimicry, bystander activation, polyclonal B-cell activation). (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3)

Risk factors for relapsing course (prognostic): higher MOG-IgG titers and persistence of seropositivity are associated with relapsing disease; relapses cluster early and can follow steroid taper/cessation. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 10-11, alani2023myelinoligodendrocyteglycoprotein pages 10-11)

2.3 Protective factors

Seroconversion to MOG-IgG negativity is associated with a lower relapse likelihood (e.g., ~90% likelihood of monophasic course in one 2024 review). (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 10-11)

2.4 Gene–environment interactions

No robust gene–environment interaction evidence was extractable from the retrieved sources in this run.

3. Phenotypes

3.1 Core clinical phenotypes (with frequency/characteristics)

MOGAD is defined by a compatible core demyelinating event, commonly including optic neuritis, myelitis, ADEM, brain/brainstem syndromes, and cortical encephalitis (often with seizures). (alani2023myelinoligodendrocyteglycoprotein pages 8-9, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10)

Optic neuritis (ON) - Frequency: most common initial adult manifestation ~30–60%. (jeyakumar2024mogantibodyassociatedoptic pages 1-2) - Common distinguishing features: bilateral involvement, disc swelling, longitudinally extensive optic nerve hyperintensity, optic perineuritis. (jeyakumar2024mogantibodyassociatedoptic pages 1-2, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10)

Transverse myelitis (TM) - Frequency: ~10–25% (one review) to ~30% (another review) in adults. (jeyakumar2024mogantibodyassociatedoptic pages 1-2, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 4-5) - Spinal cord features include LETM and gray-matter–predominant “H-sign” lesions; conus involvement is common. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 5-7, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 7-8)

Acute disseminated encephalomyelitis (ADEM) - Frequency: common in children, ~45% in children <11 years in one review; >50% in children <11 in another review. (jeyakumar2024mogantibodyassociatedoptic pages 1-2, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 4-5)

Cortical encephalitis / FLAMES - Reported phenotype characterized by unilateral cortical FLAIR hyperintensity and focal seizures that may generalize. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 3-4, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 5-7)

3.2 Suggested HPO terms (examples; not exhaustive)

(Provided as ontology suggestions; not verified against HPO database during this run.) - Optic neuritis: HP:0000648 (Optic neuritis) - Visual impairment: HP:0000505 (Visual impairment) - Transverse myelitis / myelitis: HP:0002303 (Myelitis) / HP:0002375 (Transverse myelitis) - Paraparesis/quadriparesis: HP:0003401 (Paraparesis) / HP:0002376 (Quadriplegia) - Bladder dysfunction: HP:0000010 (Neurogenic bladder) - Seizures: HP:0001250 (Seizures) - Encephalopathy: HP:0001298 (Encephalopathy) - Headache: HP:0002315 (Headache)

3.3 Quality of life impact

Direct QoL instruments/results specific to MOGAD were not extractable from the obtained papers; however, relapse-driven disability is repeatedly emphasized, and QoL is an endpoint in ongoing interventional trials (e.g., EQ-5D-3L in NCT05349006). (NCT05349006 chunk 1)

4. Genetic/Molecular Information

4.1 Causal genes / inheritance

MOGAD is not established as a monogenic disorder; no causal germline variants were supported by retrieved evidence in this run. (alani2023myelinoligodendrocyteglycoprotein pages 3-4, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3)

4.2 Pathogenic variants, modifier genes, epigenetics

No validated pathogenic variants, modifier genes, or epigenetic drivers were extractable from the retrieved evidence in this run.

4.3 Molecular target

MOG is a CNS myelin/oligodendrocyte surface protein with an extracellular Ig-like domain that is immunogenic and accessible to antibodies. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3)

5. Environmental Information

5.1 Environmental/lifestyle factors

No specific toxins/pollution/lifestyle factors were supported by retrieved evidence in this run.

5.2 Infectious agents (triggering)

Infections are proposed triggers via immune activation/molecular mimicry; specific pathogen-level causality remains uncertain in the retrieved evidence. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3)

6. Mechanism / Pathophysiology

6.1 Causal chain (current model)

A convergent contemporary model is: 1) Peripheral activation of MOG-reactive B cells/plasma cells (sometimes after systemic inflammation/infection) → generation of MOG-IgG (often IgG1). (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3, abraham2024myelinoligodendrocyteantibody pages 29-31) 2) CNS barrier dysfunction (BBB/blood–CSF barrier) enables entry of MOG-IgG and immune cells. (abraham2024myelinoligodendrocyteantibody pages 8-10, abraham2024myelinoligodendrocyteantibody pages 5-8) 3) Antibody binds conformational extracellular epitopes of MOG on myelin/oligodendrocytes and triggers effector mechanisms including complement activation, ADCC/ADCP, and downstream oligodendrocyte signaling/cytoskeletal disruption → inflammatory demyelination with perivenous/confluent lesion architecture. (abraham2024myelinoligodendrocyteantibody pages 10-13, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3, abraham2024myelinoligodendrocyteantibody pages 5-8, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 3-4) 4) Clinical manifestations depend on site of demyelination (optic nerve, spinal cord, brain/cortex). (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 5-7)

6.2 Key pathways and processes

• Complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP) are described as candidate effector mechanisms. (abraham2024myelinoligodendrocyteantibody pages 10-13, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3)
• Intracellular signaling perturbations in oligodendrocytes (e.g., MAPK/AKT) and cytoskeletal disruption are described as possible downstream mechanisms. (abraham2024myelinoligodendrocyteantibody pages 10-13)

6.3 Suggested GO biological process terms (examples)

(Ontology suggestions; not database-validated in this run.) - GO:0006955 immune response - GO:0006954 inflammatory response - GO:0002443 leukocyte mediated immunity - GO:0002250 adaptive immune response - GO:0002252 immune effector process - GO:0002479 antigen processing and presentation - GO:0002526 acute inflammatory response - GO:0006935 chemotaxis (for recruited myeloid cells) - GO:0006898 receptor-mediated endocytosis / phagocytosis-related terms (for ADCP)

6.4 Cell types involved (suggested CL terms)

(Ontology suggestions; not database-validated in this run.) - Oligodendrocyte: CL:0000128 - Microglia: CL:0000129 - Macrophage: CL:0000235 - CD4-positive T cell: CL:0000624 - B cell / plasma cell: CL:0000236 / CL:0000786

7. Anatomical Structures Affected

7.1 Organ and system level

Primary: central nervous system—optic nerves, spinal cord, brain (including cortex in FLAMES), brainstem/cerebellar pathways. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 5-7)

7.2 Suggested UBERON terms (examples)

(Ontology suggestions; not database-validated in this run.) - Optic nerve: UBERON:0000940 - Spinal cord: UBERON:0002240 - Brain: UBERON:0000955 - Cerebral cortex: UBERON:0000956

7.3 Subcellular localization

Pathogenic binding occurs at the cell surface of myelin/oligodendrocytes (MOG is on outermost myelin). (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3)

8. Temporal Development

8.1 Onset

MOGAD can present in childhood or adulthood with acute/subacute demyelinating attacks; age distribution is biphasic (5–10 years; 20–45 years). (jeyakumar2024mogantibodyassociatedoptic pages 1-2)

8.2 Progression and course

MOGAD can be monophasic or relapsing; a 2024 review summarized ~65% monophasic and ~35% relapsing. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10)

Relapses tend to occur early (often within 6–12 months) and are frequently temporally associated with steroid taper/cessation. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 10-11, wolf2023emergingprinciplesfor pages 4-6)

9. Inheritance and Population

9.1 Epidemiology (recent estimates)

From a 2024 neuro-ophthalmology review: - Annual incidence: ~1.6–4.8 per million - Prevalence: ~1.3–2.5 per 100,000 - Biphasic age peaks: 5–10 years and 20–45 years; median onset ~20–30 years - Sex ratio: approximately F:M 1:1 (with another review suggesting slight female predominance ~1.5:1). (jeyakumar2024mogantibodyassociatedoptic pages 1-2, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 7-8)

10. Diagnostics

10.1 Diagnostic criteria (2023 International MOGAD Panel)

Multiple 2024 validation studies and reviews summarize a three-step diagnostic logic: 1) Identify a core clinical demyelinating event (e.g., ON, TM, ADEM, brain/brainstem/cerebellar syndrome, cortical encephalitis with seizures). (alani2023myelinoligodendrocyteglycoprotein pages 8-9, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10) 2) Demonstrate MOG-IgG positivity (preferably in serum) using a cell-based assay, ideally a live CBA using full-length human MOG. (alani2023myelinoligodendrocyteglycoprotein pages 3-4, forcadela2024timingofmogigg pages 1-2) 3) Exclude alternative diagnoses (especially MS and AQP4-IgG NMOSD). (voase2024diagnosticcriteriafor pages 1-2, forcadela2024timingofmogigg pages 1-2)

Low-positive or ambiguous serology requires supportive clinical/MRI evidence. (alani2023myelinoligodendrocyteglycoprotein pages 8-9, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10)

A cropped table from a 2023 review that reproduces the criteria is provided in the evidence base. (alani2023myelinoligodendrocyteglycoprotein media 796e2466)

10.2 Assay methodology and interpretation (titer/PPV)

• Cell-based assays are emphasized; ELISA is discouraged due to lower specificity and discordance. (alani2023myelinoligodendrocyteglycoprotein pages 3-4)
• PPV varies strongly by titer and by testing population. One 2024 study reported PPV of MOG-IgG “at any time” 78.3% overall, 52.6% for low titer, 90.1% for high titer, and much higher PPV in children vs adults. (varley2024validationofthe pages 1-2)
• Reviews summarize that low titers can generate false positives and require careful clinical/MRI correlation. (alani2023myelinoligodendrocyteglycoprotein pages 3-4, rechtman2024assessingtheapplicability pages 1-2, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 7-8)

10.3 Supportive MRI/CSF features

Supportive imaging features (particularly important for low-positive results) include: bilateral ON, >50% optic nerve involvement, optic disc edema, optic perineuritis; LETM, central cord/H-sign, conus involvement; fluffy, poorly demarcated deep gray/cortical/brainstem lesions. (alani2023myelinoligodendrocyteglycoprotein pages 8-9, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 5-7, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 7-8)

CSF: pleocytosis and elevated protein in ~50%; oligoclonal bands uncommon (<10–15%). (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 7-8)

10.4 Diagnostic accuracy and validation (2024)

• Varley et al. (Neurology; 2024-07) reported high performance of the 2023 criteria in a selected cohort: sensitivity 96.5%, specificity 98.9%, PPV 94.3%, NPV 99.3%, accuracy 98.5%. (https://doi.org/10.1212/WNL.0000000000209321) (varley2024validationofthe pages 1-2)
• Forcadela et al. (NNI; 2024-01) emphasized timing: low-positive results correlate with delayed sampling and criteria can miss cases if testing is delayed or investigations are incomplete; they report sensitivity 97% and specificity 100% in their cohort. (https://doi.org/10.1212/nxi.0000000000200183) (forcadela2024timingofmogigg pages 1-2)

11. Outcome / Prognosis

11.1 Disability and relapse contribution

Reviews emphasize that relapses are a major driver of disability and that predicting relapse at diagnosis remains difficult; persistent seropositivity and high titers support higher relapse risk. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 10-11, alani2023myelinoligodendrocyteglycoprotein pages 10-11)

11.2 Prognostic biomarkers (candidate)

A 2024 review summarizes multiple candidate predictors (none fully validated): persistent seropositivity at 3 months, higher titers, certain epitope specificities, CSF protein/leukocytes, PLR, serum neurofilament light chain, polyphasic first attack, comorbid immunologic disease. (abraham2024myelinoligodendrocyteantibody pages 27-29)

12. Treatment

12.1 Acute relapse treatment (real-world implementation)

Corticosteroids are first-line and MOGAD attacks are typically highly steroid responsive; an extended taper is commonly used to mitigate early relapse risk. (alani2023myelinoligodendrocyteglycoprotein pages 9-10, wolf2023emergingprinciplesfor pages 4-6)

Quantitative observational outcomes: - A retrospective dataset summarized in Wolf et al. (2023-11) reported outcomes after IVMP across 122 relapses: 50% complete/nearly complete recovery, 44.3% partial recovery, 7% minimal/no recovery. (https://doi.org/10.1007/s11940-023-00776-1) (wolf2023emergingprinciplesfor pages 3-4) - A review summarized a retrospective comparison with response rates 96% IVMP, 90% PLEX, 91% IVIG. (abraham2024myelinoligodendrocyteantibody pages 17-20)

Second-line/adjunct in refractory or severe attacks: plasma exchange (PLEX) and IVIG. (wolf2023emergingprinciplesfor pages 3-4)

12.2 Maintenance (relapse prevention; off-label practice)

Commonly considered after ≥2 attacks, with some experts considering earlier in severe poor-recovery cases. (wolf2023emergingprinciplesfor pages 4-6)

Evidence synthesis (observational): - IVIG: multicenter cohort summarized by Wolf et al. shows ARR reduction 1.4 → 0.39; relapse occurred in 34% overall but 17% with ≥1 g/kg every 4 weeks; only 3% discontinued due to adverse events. (wolf2023emergingprinciplesfor pages 6-8) - Azathioprine (AZA) / Mycophenolate mofetil (MMF): may reduce ARR in some retrospective series but up to ~50% relapse; delayed onset (3–6 months) often requires bridging with steroids; notable safety monitoring needs (e.g., TPMT testing for AZA). (wolf2023emergingprinciplesfor pages 6-8, wolf2023emergingprinciplesfor pages 4-6) - Rituximab (anti-CD20): meta-analytic support for ARR reduction, but potentially less effective than in AQP4+ NMOSD; relapses may occur without link to B-cell repletion. (wolf2023emergingprinciplesfor pages 6-8) - IL-6 receptor blockade (tocilizumab/satralizumab): biologically plausible with supportive retrospective series; Wolf et al. note retrospective series with relapse reduction and report (largest series) 73% relapse-free >1 year. (wolf2023emergingprinciplesfor pages 8-9) - FcRn inhibition (rozanolixizumab): rationale is reducing pathogenic IgG by blocking FcRn-mediated IgG recycling; now being tested in phase 3. (wolf2023emergingprinciplesfor pages 8-9, gklinos2024myelinoligodendrocyteglycoproteinantibody pages 11-13)

12.3 Treatment ontology suggestions (MAXO; examples)

(Ontology suggestions; not database-validated in this run.) - High-dose corticosteroid therapy: MAXO term for systemic glucocorticoid therapy - Plasma exchange: MAXO term for therapeutic plasma exchange - Intravenous immunoglobulin therapy: MAXO term for IVIG administration - Anti-CD20 monoclonal antibody therapy (rituximab) - Immunosuppressive therapy (azathioprine, mycophenolate) - Anti–IL-6 receptor therapy (tocilizumab, satralizumab) - FcRn inhibitor therapy (rozanolixizumab)

13. Prevention

No established primary prevention exists; secondary/tertiary prevention focuses on: - Accurate diagnosis (avoid false positives/overdiagnosis due to low titers and non-specific testing). (alani2023myelinoligodendrocyteglycoprotein pages 3-4, varley2024validationofthe pages 1-2, rechtman2024assessingtheapplicability pages 1-2) - Relapse prevention using prolonged steroid taper and/or maintenance immunotherapy in relapsing disease. (wolf2023emergingprinciplesfor pages 4-6, wolf2023emergingprinciplesfor pages 6-8)

14. Other Species / Natural Disease

No naturally occurring veterinary MOGAD analog evidence was retrieved in this run.

15. Model Organisms

Mechanistic work includes animal model evidence that anti-MOG antibodies can be pathogenic in the presence of myelin-reactive T cells; translation is complicated because many human MOG antibodies do not bind rodent MOG. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3)

Recent developments (2023–2024 emphasis)

1) Formal diagnostic criteria (2023) and real-world validation (2024): Multiple 2024 studies report high sensitivity/specificity and highlight timing and supportive-feature requirements for low-positive titers. (forcadela2024timingofmogigg pages 1-2, varley2024validationofthe pages 1-2, rechtman2024assessingtheapplicability pages 1-2) 2) Quantitative emphasis on test interpretation: 2024 PPV analysis shows marked drop in PPV for low titers and for patients lacking a core demyelinating attack. (varley2024validationofthe pages 1-2) 3) Shift toward targeted relapse-prevention trials: Phase 3 trials are actively evaluating FcRn inhibition (rozanolixizumab) and IL-6 blockade (satralizumab); a phase 3 immunosuppressant strategy trial (azathioprine) and a randomized tocilizumab trial are ongoing. (NCT05063162 chunk 1, NCT05271409 chunk 1, NCT05349006 chunk 1, NCT06452537 chunk 1)

Current applications and real-world implementations

• Standard of care in most centers uses high-dose steroids for acute attacks, early escalation to IVIG/PLEX if poor response, and individualized relapse-prevention therapy (often IVIG, AZA/MMF, rituximab, with increasing interest in IL-6 blockade). (wolf2023emergingprinciplesfor pages 3-4, wolf2023emergingprinciplesfor pages 6-8, wolf2023emergingprinciplesfor pages 8-9)
• Monitoring: serial MOG-IgG titers are sometimes followed; seronegativity by ~12 months is associated with monophasic course in one review (but later re-positivity can occur). (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 10-11)

Expert opinion / analysis (authoritative sources)

• Diagnostic caution is repeatedly stressed: testing is meaningful only with compatible phenotype and imaging, and low titers require careful weighting because PPV depends on pretest probability and population prevalence. (alani2023myelinoligodendrocyteglycoprotein pages 3-4, varley2024validationofthe pages 1-2)
• Treatment evidence remains dominated by retrospective cohorts; expert reviews emphasize the urgent need for RCTs and biomarkers to guide long-term immunotherapy decisions. (wolf2023emergingprinciplesfor pages 8-9, abraham2024myelinoligodendrocyteantibody pages 20-22)

Key statistics (selected)

• Incidence: 1.6–4.8 per million/year; prevalence: 1.3–2.5 per 100,000. (jeyakumar2024mogantibodyassociatedoptic pages 1-2)
• Biphasic age peaks: 5–10 years and 20–45 years; median onset ~20–30 years. (jeyakumar2024mogantibodyassociatedoptic pages 1-2)
• Course: ~65% monophasic / 35% relapsing (review summary). (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10)
• CSF: pleocytosis ~50%; oligoclonal bands <10–15%. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 7-8)
• Diagnostic criteria validation (2024): sensitivity 96.5%, specificity 98.9% (selected cohort). (varley2024validationofthe pages 1-2)
• Acute IVMP outcomes (retrospective): 50% complete/nearly complete recovery, 44.3% partial, 7% minimal/no recovery. (wolf2023emergingprinciplesfor pages 3-4)
• IVIG maintenance (multicenter cohort summary): ARR 1.4 → 0.39; relapse on IVIG 34% overall, 17% with ≥1 g/kg q4w; AE discontinuation 3%. (wolf2023emergingprinciplesfor pages 6-8)

Visual evidence: 2023 criteria table

A cropped table summarizing the 2023 International MOGAD Panel diagnostic criteria (core clinical events, titer thresholds, and supportive features) is available from Al-Ani et al. (2023). (alani2023myelinoligodendrocyteglycoprotein media 796e2466)

Structured summary artifact

Table: This table condenses high-yield disease characteristics of MOGAD for knowledge-base use, including 2023 diagnostic criteria, major phenotypes, epidemiology, pathophysiology, treatment evidence, and ongoing interventional trials.

Ongoing interventional trials (ClinicalTrials.gov; real-world implementation pipeline)

• NCT05271409 (METEOROID; satralizumab) – Phase 3, randomized double-blind placebo-controlled, recruiting; primary endpoint: time to first adjudicated relapse; estimated n≈152; ages ≥12. (Record sponsor: Hoffmann-La Roche; start 2022; URL: https://clinicaltrials.gov/study/NCT05271409) (NCT05271409 chunk 1)
• NCT05063162 (cosMOG; rozanolixizumab) – Phase 3, randomized double-blind with open-label extension; ACTIVE_NOT_RECRUITING; enrolled 113; primary endpoint: time to first centrally adjudicated relapse. (Sponsor: UCB Biopharma SRL; start 2022-02-02; URL: https://clinicaltrials.gov/study/NCT05063162) (NCT05063162 chunk 1)
• NCT05349006 (Azathioprine in MOGAD) – Phase 3, placebo-controlled, recruiting; first-attack adults; primary endpoint: time to first relapse up to 3 years; includes EQ-5D-3L QoL endpoint. (Sponsor: Hospices Civils de Lyon; start 2023-12-12; URL: https://clinicaltrials.gov/study/NCT05349006) (NCT05349006 chunk 1)
• NCT06452537 (Tocilizumab in MOGAD) – Phase 2/3, randomized open-label, ACTIVE_NOT_RECRUITING; n≈102; primary endpoint: time to first adjudicated relapse. (Sponsor: Tianjin Medical University General Hospital; start 2024-07-09; URL: https://clinicaltrials.gov/study/NCT06452537) (NCT06452537 chunk 1)

Limitations of this report (data availability)

• ICD/MeSH/Orphanet/OMIM identifiers and PMIDs were not directly retrievable from the tool-accessible snippets, so these could not be exhaustively enumerated. (NCT05271409 chunk 3)
• Several mechanistic/pathology statements are based on 2024 narrative reviews (including one with incomplete bibliographic metadata in the retrieved record), and should be cross-checked against primary pathology papers for formal knowledge-base curation. (abraham2024myelinoligodendrocyteantibody pages 10-13, abraham2024myelinoligodendrocyteantibody pages 1-5)

References

1. (voase2024diagnosticcriteriafor pages 1-2): Sophie Voase and Neil P. Robertson. Diagnostic criteria for mogad. Journal of Neurology, 271:3690-3692, May 2024. URL: https://doi.org/10.1007/s00415-024-12405-1, doi:10.1007/s00415-024-12405-1. This article has 4 citations and is from a domain leading peer-reviewed journal.

2. (alani2023myelinoligodendrocyteglycoprotein pages 3-4): Abdullah Al-Ani, John J. Chen, and Fiona Costello. Myelin oligodendrocyte glycoprotein antibody-associated disease (mogad): current understanding and challenges. Journal of Neurology, 270:1-19, May 2023. URL: https://doi.org/10.1007/s00415-023-11737-8, doi:10.1007/s00415-023-11737-8. This article has 72 citations and is from a domain leading peer-reviewed journal.

3. (jeyakumar2024mogantibodyassociatedoptic pages 1-2): Niroshan Jeyakumar, Magdalena Lerch, Russell C. Dale, and Sudarshini Ramanathan. Mog antibody-associated optic neuritis. Eye, 38:2289-2301, May 2024. URL: https://doi.org/10.1038/s41433-024-03108-y, doi:10.1038/s41433-024-03108-y. This article has 67 citations and is from a peer-reviewed journal.

4. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 1-3): Panagiotis Gklinos and Ruth Dobson. Myelin oligodendrocyte glycoprotein-antibody associated disease: an updated review of the clinical spectrum, pathogenetic mechanisms and therapeutic management. Antibodies, 13:43, May 2024. URL: https://doi.org/10.3390/antib13020043, doi:10.3390/antib13020043. This article has 24 citations.

5. (forcadela2024timingofmogigg pages 1-2): Mirasol Forcadela, Chiara Rocchi, Daniel San Martin, Emily L. Gibbons, Daniel Wells, Mark R. Woodhall, Patrick J. Waters, Saif Huda, and Shahd Hamid. Timing of mog-igg testing is key to 2023 mogad diagnostic criteria. Neurology Neuroimmunology & Neuroinflammation, Jan 2024. URL: https://doi.org/10.1212/nxi.0000000000200183, doi:10.1212/nxi.0000000000200183. This article has 54 citations.

6. (NCT05271409 chunk 3): A Study to Evaluate the Efficacy, Safety, Pharmacokinetics, and Pharmacodynamics of Satralizumab in Participants With Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease. Hoffmann-La Roche. 2022. ClinicalTrials.gov Identifier: NCT05271409

7. (varley2024validationofthe pages 1-2): James A. Varley, Dimitrios Champsas, Timothy Prossor, Giuseppe Pontillo, Omar Abdel-Mannan, Zhaleh Khaleeli, Axel Petzold, Ahmed T. Toosy, Sachid A. Trip, Heather Wilson, Dermot H. Mallon, Cheryl Hemingway, Kshitij Mankad, Michael Kin Loon Chou, Andrew J. Church, Melanie S. Hart, Michael P. Lunn, Wallace Brownlee, Yael Hacohen, and Olga Ciccarelli. Validation of the 2023 international diagnostic criteria for mogad in a selected cohort of adults and children. Neurology, Jul 2024. URL: https://doi.org/10.1212/wnl.0000000000209321, doi:10.1212/wnl.0000000000209321. This article has 33 citations and is from a highest quality peer-reviewed journal.

8. (NCT05063162 chunk 1): A Study to Evaluate the Efficacy and Safety of Rozanolixizumab in Adult Participants With Myelin Oligodendrocyte Glycoprotein (MOG) Antibody-associated Disease (MOGAD). UCB Biopharma SRL. 2022. ClinicalTrials.gov Identifier: NCT05063162

9. (NCT05271409 chunk 1): A Study to Evaluate the Efficacy, Safety, Pharmacokinetics, and Pharmacodynamics of Satralizumab in Participants With Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease. Hoffmann-La Roche. 2022. ClinicalTrials.gov Identifier: NCT05271409

10. (abraham2024myelinoligodendrocyteantibody pages 10-13): F Abraham. Myelin oligodendrocyte antibody associated disease (mogad): a review of mechanisms, clinical features, pathology, and new …. Unknown journal, 2024.

11. (abraham2024myelinoligodendrocyteantibody pages 8-10): F Abraham. Myelin oligodendrocyte antibody associated disease (mogad): a review of mechanisms, clinical features, pathology, and new …. Unknown journal, 2024.

12. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 10-11): Panagiotis Gklinos and Ruth Dobson. Myelin oligodendrocyte glycoprotein-antibody associated disease: an updated review of the clinical spectrum, pathogenetic mechanisms and therapeutic management. Antibodies, 13:43, May 2024. URL: https://doi.org/10.3390/antib13020043, doi:10.3390/antib13020043. This article has 24 citations.

13. (alani2023myelinoligodendrocyteglycoprotein pages 10-11): Abdullah Al-Ani, John J. Chen, and Fiona Costello. Myelin oligodendrocyte glycoprotein antibody-associated disease (mogad): current understanding and challenges. Journal of Neurology, 270:1-19, May 2023. URL: https://doi.org/10.1007/s00415-023-11737-8, doi:10.1007/s00415-023-11737-8. This article has 72 citations and is from a domain leading peer-reviewed journal.

14. (alani2023myelinoligodendrocyteglycoprotein pages 8-9): Abdullah Al-Ani, John J. Chen, and Fiona Costello. Myelin oligodendrocyte glycoprotein antibody-associated disease (mogad): current understanding and challenges. Journal of Neurology, 270:1-19, May 2023. URL: https://doi.org/10.1007/s00415-023-11737-8, doi:10.1007/s00415-023-11737-8. This article has 72 citations and is from a domain leading peer-reviewed journal.

15. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 8-10): Panagiotis Gklinos and Ruth Dobson. Myelin oligodendrocyte glycoprotein-antibody associated disease: an updated review of the clinical spectrum, pathogenetic mechanisms and therapeutic management. Antibodies, 13:43, May 2024. URL: https://doi.org/10.3390/antib13020043, doi:10.3390/antib13020043. This article has 24 citations.

16. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 4-5): Panagiotis Gklinos and Ruth Dobson. Myelin oligodendrocyte glycoprotein-antibody associated disease: an updated review of the clinical spectrum, pathogenetic mechanisms and therapeutic management. Antibodies, 13:43, May 2024. URL: https://doi.org/10.3390/antib13020043, doi:10.3390/antib13020043. This article has 24 citations.

17. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 5-7): Panagiotis Gklinos and Ruth Dobson. Myelin oligodendrocyte glycoprotein-antibody associated disease: an updated review of the clinical spectrum, pathogenetic mechanisms and therapeutic management. Antibodies, 13:43, May 2024. URL: https://doi.org/10.3390/antib13020043, doi:10.3390/antib13020043. This article has 24 citations.

18. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 7-8): Panagiotis Gklinos and Ruth Dobson. Myelin oligodendrocyte glycoprotein-antibody associated disease: an updated review of the clinical spectrum, pathogenetic mechanisms and therapeutic management. Antibodies, 13:43, May 2024. URL: https://doi.org/10.3390/antib13020043, doi:10.3390/antib13020043. This article has 24 citations.

19. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 3-4): Panagiotis Gklinos and Ruth Dobson. Myelin oligodendrocyte glycoprotein-antibody associated disease: an updated review of the clinical spectrum, pathogenetic mechanisms and therapeutic management. Antibodies, 13:43, May 2024. URL: https://doi.org/10.3390/antib13020043, doi:10.3390/antib13020043. This article has 24 citations.

20. (NCT05349006 chunk 1): Azathioprine in MOGAD. Hospices Civils de Lyon. 2023. ClinicalTrials.gov Identifier: NCT05349006

21. (abraham2024myelinoligodendrocyteantibody pages 29-31): F Abraham. Myelin oligodendrocyte antibody associated disease (mogad): a review of mechanisms, clinical features, pathology, and new …. Unknown journal, 2024.

22. (abraham2024myelinoligodendrocyteantibody pages 5-8): F Abraham. Myelin oligodendrocyte antibody associated disease (mogad): a review of mechanisms, clinical features, pathology, and new …. Unknown journal, 2024.

23. (wolf2023emergingprinciplesfor pages 4-6): Andrew B. Wolf, Jacqueline Palace, and Jeffrey L. Bennett. Emerging principles for treating myelin oligodendrocyte glycoprotein antibody-associated disease (mogad). Current Treatment Options in Neurology, 25:437-453, Nov 2023. URL: https://doi.org/10.1007/s11940-023-00776-1, doi:10.1007/s11940-023-00776-1. This article has 5 citations and is from a peer-reviewed journal.

24. (alani2023myelinoligodendrocyteglycoprotein media 796e2466): Abdullah Al-Ani, John J. Chen, and Fiona Costello. Myelin oligodendrocyte glycoprotein antibody-associated disease (mogad): current understanding and challenges. Journal of Neurology, 270:1-19, May 2023. URL: https://doi.org/10.1007/s00415-023-11737-8, doi:10.1007/s00415-023-11737-8. This article has 72 citations and is from a domain leading peer-reviewed journal.

25. (rechtman2024assessingtheapplicability pages 1-2): Ariel Rechtman, Tal Freidman-Korn, Omri Zveik, Lyne Shweiki, Garrick Hoichman, and Adi Vaknin-Dembinsky. Assessing the applicability of the 2023 international mogad panel criteria in real-world clinical settings. Journal of Neurology, 271:5102-5108, May 2024. URL: https://doi.org/10.1007/s00415-024-12438-6, doi:10.1007/s00415-024-12438-6. This article has 10 citations and is from a domain leading peer-reviewed journal.

26. (abraham2024myelinoligodendrocyteantibody pages 27-29): F Abraham. Myelin oligodendrocyte antibody associated disease (mogad): a review of mechanisms, clinical features, pathology, and new …. Unknown journal, 2024.

27. (alani2023myelinoligodendrocyteglycoprotein pages 9-10): Abdullah Al-Ani, John J. Chen, and Fiona Costello. Myelin oligodendrocyte glycoprotein antibody-associated disease (mogad): current understanding and challenges. Journal of Neurology, 270:1-19, May 2023. URL: https://doi.org/10.1007/s00415-023-11737-8, doi:10.1007/s00415-023-11737-8. This article has 72 citations and is from a domain leading peer-reviewed journal.

28. (wolf2023emergingprinciplesfor pages 3-4): Andrew B. Wolf, Jacqueline Palace, and Jeffrey L. Bennett. Emerging principles for treating myelin oligodendrocyte glycoprotein antibody-associated disease (mogad). Current Treatment Options in Neurology, 25:437-453, Nov 2023. URL: https://doi.org/10.1007/s11940-023-00776-1, doi:10.1007/s11940-023-00776-1. This article has 5 citations and is from a peer-reviewed journal.

29. (abraham2024myelinoligodendrocyteantibody pages 17-20): F Abraham. Myelin oligodendrocyte antibody associated disease (mogad): a review of mechanisms, clinical features, pathology, and new …. Unknown journal, 2024.

30. (wolf2023emergingprinciplesfor pages 6-8): Andrew B. Wolf, Jacqueline Palace, and Jeffrey L. Bennett. Emerging principles for treating myelin oligodendrocyte glycoprotein antibody-associated disease (mogad). Current Treatment Options in Neurology, 25:437-453, Nov 2023. URL: https://doi.org/10.1007/s11940-023-00776-1, doi:10.1007/s11940-023-00776-1. This article has 5 citations and is from a peer-reviewed journal.

31. (wolf2023emergingprinciplesfor pages 8-9): Andrew B. Wolf, Jacqueline Palace, and Jeffrey L. Bennett. Emerging principles for treating myelin oligodendrocyte glycoprotein antibody-associated disease (mogad). Current Treatment Options in Neurology, 25:437-453, Nov 2023. URL: https://doi.org/10.1007/s11940-023-00776-1, doi:10.1007/s11940-023-00776-1. This article has 5 citations and is from a peer-reviewed journal.

32. (gklinos2024myelinoligodendrocyteglycoproteinantibody pages 11-13): Panagiotis Gklinos and Ruth Dobson. Myelin oligodendrocyte glycoprotein-antibody associated disease: an updated review of the clinical spectrum, pathogenetic mechanisms and therapeutic management. Antibodies, 13:43, May 2024. URL: https://doi.org/10.3390/antib13020043, doi:10.3390/antib13020043. This article has 24 citations.

33. (NCT06452537 chunk 1): Chao Zhang. Safety and Efficacy of Tocilizumab in Patients With Myelin Oligodendrocyte Glycoprotein Antibody-associated Disease. Tianjin Medical University General Hospital. 2024. ClinicalTrials.gov Identifier: NCT06452537

34. (abraham2024myelinoligodendrocyteantibody pages 20-22): F Abraham. Myelin oligodendrocyte antibody associated disease (mogad): a review of mechanisms, clinical features, pathology, and new …. Unknown journal, 2024.

35. (abraham2024myelinoligodendrocyteantibody pages 1-5): F Abraham. Myelin oligodendrocyte antibody associated disease (mogad): a review of mechanisms, clinical features, pathology, and new …. Unknown journal, 2024.