Myelin Oligodendrocyte Glycoprotein (MOG) Antibody Disease [MOG-AD]

1. Myelin oligodendrocyte glycoprotein (MOG)
antibody disease (MOG-AD)
Ade Wijaya, MD – September 2020

2. Myelin Oligodendrocyte Glycoprotein
(MOG)
• is a glycoprotein located on the myelin surface and found
exclusively in the central nervous system (CNS)
• Functions: cellular adhesive molecule, to be involved as a
regulator of oligodendrocyte microtubule stability and to
mediate complement cascade
Schluesener H et al (1987) A monoclonal antibody against a myelin oligodendrocyte glycoprotein induces relapses and demyelination in central nervous system autoimmune disease. J Immunol 139(12):4016–4021
Bernard C et al (1997) Myelin oligodendrocyte glycoprotein: a novel candidate autoantigen in multiple sclerosis. J Mol Med 75(2):77–88
Johns T, Bernard C (1999) The structure and function of myelin oligodendrocyte glycoprotein. J Neurochem 72(1):1–9

3. Introduction
• MOG antibodies have been extensively studied over the last 30
years, with some early experimental studies hypothesizing a
pathogenic role in CNS inflammatory diseases
• The more recent development of highly sensitive and specific
methods for MOG antibody detection using cell-based assays,
along with new diagnostic classification of similar
neuroinflammatory conditions, has made it possible to identify a
subset of patients with antibodies to MOG who express a clinical
phenotype distinct from MS or from neuromyelitis optica (NMO)
Wynford-Thomas R, Jacob A, Tomassini V. Neurological update: MOG antibody disease. Journal of neurology. 2019 May 1;266(5):1280-6.

4. Wynford-Thomas R, Jacob A, Tomassini V. Neurological update: MOG antibody disease. Journal of neurology. 2019 May 1;266(5):1280-6.

5. When to Test for MOG Antibody
Test if
• Clinical/paraclinical features are suggestive of MOG-AD (2018 International
Recommendations)
• Diagnosis of MS is made, interferon beta or natalizumab has been started, but efficacy
is unexpectedly poor and clinical/paraclinical features are compatible with MOG-AD
Re-test if
• MOG antibody positive, but clinical/paraclinical features not suggestive of MOG-AD
(see “MOG antibody positivity and the diagnosis of MOG-AD: “red flags””)
• Clinical/paraclinical features continue to be suggestive of MOG-AD, but MOG antibody
is negative. Likelihood of further events is sought, following MOG-AD diagnosis
Jarius S et al (2018) MOG encephalomyelitis: international recommendations on diagnosis and antibody testing. J Neuroinflamm 15:134

6. Biopsy
• Compatible with pattern II histopathology of MS, i.e., with
lesions presenting complement and IgG deposits at the sites
of ongoing demyelination
Jarius S et al (2016) Screening for MOG-IgG and 27 other antiglial and anti-neuronal autoantibodies in ‘pattern II multiple sclerosis’ and brain biopsy findings in a MOG-IgG-positive case. Mult Scler J 22(12):1541–1549
Spadaro M et al (2015) Histopathology and clinical course of MOG-antibody-associated encephalomyelitis. Ann Clin Transl Neurol 2(3):295–301

7. Management
Wynford-Thomas R, Jacob A, Tomassini V. Neurological update: MOG antibody disease. Journal of neurology. 2019 May 1;266(5):1280-6.

8. Summary
• The diagnosis of MOG-AD is crucial to plan appropriate
management
• Suggestive clinical and paraclinical features, in association
with MOG antibody positivity, aid the identification of MOG-
AD from other inflammatory demyelinating diseases

9. THANK YOU