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Review
. 2024 May 17;13(2):43.
doi: 10.3390/antib13020043.

Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management

Panagiotis Gklinos  1 , Ruth Dobson  2
Affiliations
Review

Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease: An Updated Review of the Clinical Spectrum, Pathogenetic Mechanisms and Therapeutic Management

Panagiotis Gklinos et al. Antibodies (Basel). .

Abstract

Clinical syndromes associated with antibodies against myelin oligodendrocyte glycoprotein (MOG) are now recognized as a distinct neurological disease entity, and are gaining increasing attention. The pathogenic mechanisms underlying MOG-antibody disease (MOGAD) remain incompletely understood. Case series, facilitated by registries, and observational studies over the past few years have shed increasing light on the clinical aspects and therapeutic approaches of MOGAD. MOGAD may manifest with a variety of clinical syndromes, including acute disseminated encephalomyelitis (ADEM), autoimmune encephalitis, optic neuritis (ON) and transverse myelitis (TM). MOGAD can be either monophasic or relapsing. This review aims to provide a comprehensive updated description of the clinical spectrum, paraclinical features, and prognosis of MOG-antibody disease, as well as summarize its therapeutic considerations. Randomized clinical trials, standardized diagnostic criteria and treatment guidelines are the steps forward.

Keywords: antibody; autoimmune diseases; myelin oligodendrocyte glycoprotein; neuroinflammation; neuromyelitis optica spectrum disorders.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
MOGAD pathogenesis. IL-6: Interleukin-6, IL-17: Interleukin 17, TNF-a: Tumor Necrosis Factor-a.
Figure 2
Figure 2
Recommended treatment algorithm for patients with MOGAD.
See this image and copyright information in PMC

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