Anti-MOG antibody: The history, clinical phenotype, and pathogenicity of a serum biomarker for demyelination

Ramanathan, Sudarshini; Dale, Russell C.; Brilot, Fabienne

doi:10.1016/j.autrev.2015.12.004

Cited by 231 publications

(185 citation statements)

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“…MOG is expressed exclusively on the surface of oligodendrocytes in the CNS and is thought to be a late component in the development of myelin. 6 MOG was found to be an autoantigen in the experimental autoimmune encephalomyelitis model of MS in mice. 6 There is some controversy regarding phenotypic correlations of anti-MOG antibodies in humans.…”

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confidence: 99%

“…6 MOG was found to be an autoantigen in the experimental autoimmune encephalomyelitis model of MS in mice. 6 There is some controversy regarding phenotypic correlations of anti-MOG antibodies in humans. An earlier study by Sato et al 7 found that patients with MOG antibodies tended to have a more limited phenotype of mostly ON or caudal myelitis with generally better recovery from attacks and less accrual of disability than AQP4 antibody-positive patients.…”

Section: Sectionmentioning

confidence: 99%

“…Recent studies have consistently documented that some AQP4-seronegative patients with NMOSD have antibodies to MOG. 5,6 Because of frequent recurrences, at age 16 the patient was started on immunosuppressive therapy (azathioprine) for presumed seronegative NMOSD. She continued to have relapses of ON while on azathioprine and 2 years later she was switched to rituximab infusions every 6 months.…”

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confidence: 99%

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Clinical Reasoning: A patient with a history of encephalomyelitis and recurrent optic neuritis

et al. 2017

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Clinical Reasoning: A patient with a history of encephalomyelitis and recurrent optic neuritis

et al. 2017

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“…15 Patients with myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination also have a unique clinical, radiological, and therapeutic profile. 16 These examples illustrate well how the integration of clinical and biomarker data can be used to provide specific prognostic and therapeutic advice to individual patients.…”

Section: Personalised Medicine For Multiple Sclerosis: Is It Needed?mentioning

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Personalised medicine for multiple sclerosis care

2016

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Treatments with a range of efficacy and risk of adverse events have become available for the management of multiple sclerosis (MS). However, now the heterogeneity of clinical expression and responses to treatment pose major challenges to improving patient care. Selecting and managing the drug best balancing benefit and risk demands a new focus on the individual patient. Personalised medicine for MS is based on improving the precision of diagnosis for each patient in order to capture prognosis and provide an evidence-based framework for predicting treatment response and personalising patient monitoring. It involves development of predictive models involving the integration of clinical and biological data with an understanding of the impact of disease on the lives of individual patients. Here, we provide a brief, selective review of challenges to personalisation of the management of MS and suggest an agenda for stakeholder engagement and research to address them.

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“…MOG represents less than 0.05% of total myelin proteins but despite its meager concentration, it is believed to be involved in important functions, such as being a surface marker of the mature oligodendrocyte and participating in the interactions between myelin and its players 1 . The better structural characterization of MOG as well as its location rapidly made it an antigen used successfully in the induction of experimental models of demyelination such as experimental autoimmune encephalomyelitis.…”

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Anti-MOG syndrome: a road to be paved

Adoni

2017

Arq. Neuro-Psiquiatr.

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M yelin oligodendrocyte glycoprotein (MOG) is a protein expressed only on the outermost lamellae of the myelin sheath and on the surface of oligodendrocytes in the central nervous system (CNS). MOG represents less than 0.05% of total myelin proteins but despite its meager concentration, it is believed to be involved in important functions, such as being a surface marker of the mature oligodendrocyte and participating in the interactions between myelin and its players 1 . The better structural characterization of MOG as well as its location rapidly made it an antigen used successfully in the induction of experimental models of demyelination such as experimental autoimmune encephalomyelitis. Thereafter, the presence of anti-MOG antibodies was investigated in those diseases that represented the clinical prototype of demyelinating conditions: acute disseminated encephalomyelitis (ADEM) in children and multiple sclerosis (MS) in adults 2 . Although anti-MOG antibodies have been found in such prototypical situations, probably for laboratory methodological reasons, the clinical utility of antibody detection as a reliable biomarker was abandoned 3 . The development of a more specific and sensitive laboratory methodology (cell based assay, CBA) allowed to revisit the anti-MOG antibody in demyelinating diseases and to establish it as a new biomarker. To date, once the presence of the antibody in the serum has been identified, it seems reasonable to include the following entities under the anti-MOG spectrum: recurrent or bilateral optic neuritis (ON), ADEM, neuromyelitis optica spectrum disorders anti-aquaporin-4 negative and longitudinal extensive transverse myelitis 4 . Recently, Ogawa et al. described four young men with unilateral encephalitis and epileptic seizures of benign evolution and response to steroids in which the anti-MOG antibody was the only one detected.5 However, we must keep in mind that it is a knowledge still under construction, a road to be paved, particularly regarding the recognition of the whole spectrum, its long-term behavior and the best therapeutic approach.In this issue of Arquivos de Neuropsiquiatria, Costa et al. describe six patients ( four men) with optic neuritis ( five monophasic, four bilateral) and serum anti-MOG antibody in very high titers except in one case 6 . Due to the rarity of the disease, the number of anti-MOG positive patients analyzed is quite reasonable. However, the authors included a positive anti-MOG patient (patient 2) whose clinical presentation was neuritis and myelitis, which is beyond the scope of the article. Regarding the data presented, Costa et al. could have added more information regarding MRI. For example, no mention was made of the lenght of optic neuritis, which is usually greater than that found in patients with MS and even with NMOSD aquaporin 4 positive, although it is not usual to reach the optic chiasm. Another data that could be investigated would be the presence of intraorbital fat tissue contrast enhancement, a characteristic recently described and...

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Anti-MOG antibody: The history, clinical phenotype, and pathogenicity of a serum biomarker for demyelination

Cited by 231 publications

References 133 publications

Clinical Reasoning: A patient with a history of encephalomyelitis and recurrent optic neuritis

Clinical Reasoning: A patient with a history of encephalomyelitis and recurrent optic neuritis

Personalised medicine for multiple sclerosis care

Anti-MOG syndrome: a road to be paved

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