Myelin oligodendrocyte glycoprotein

Skip to content. What is myelin oligodendrocyte glycoprotein antibody disease?

Myelin oligodendrocyte glycoprotein antibody-associated disease, also known as MOGAD, is a rare inflammatory disease that affects the central nervous system. In MOGAD , the immune system attacks the fatty substance that protects nerve fibers in the optic nerves, brain and spinal cord. Symptoms of MOGAD may include vision loss, muscle weakness, stiffness or paralysis, confusion, seizures, and headaches. These symptoms can be sometimes confused with other diseases such as multiple sclerosis. However, there are treatments to help speed the recovery from attacks, manage symptoms and reduce the likelihood of symptoms returning.

Myelin oligodendrocyte glycoprotein

Federal government websites often end in. The site is secure. Data Availaiblity statement is not applicable as this review article is based exclusively on published work. New diagnostic criteria for myelin oligodendrocyte glycoprotein antibody-associated disease MOGAD have recently been proposed, distinguishing this syndrome from other inflammatory diseases of the central nervous system. Seropositivity status for MOG-IgG autoantibodies is important for diagnosing MOGAD, but only in the context of robust clinical characterization and cautious interpretation of neuroimaging. For this reason, possible alternative diagnoses need to be considered, and low MOG-IgG titers need to be carefully weighted. Key challenges to the current understanding of MOGAD are also highlighted, including uncertainty regarding the specificity and pathogenicity of MOG autoantibodies, the need to identify immunopathologic targets for future therapies, the quest to validate biomarkers that facilitate diagnosis and detect disease activity, and the importance of deciphering which patients with MOGAD require long-term immunotherapy. Myelin oligodendrocyte glycoprotein antibody-associated disease MOGAD is a relatively new addition to the category of central nervous system CNS inflammatory demyelinating diseases [ 1 , 2 ]. CNS inflammatory demyelinating conditions, including multiple sclerosis MS and neuromyelitis optica spectrum disorders NMOSD , are differentiated based on severity, clinical phenotype, imaging, laboratory, and pathological findings [ 2 ] Table 1. The current estimated range of incidence in the pediatric population is 3. Notably, these numbers, along with the estimated worldwide prevalence of 20 million [ 5 ], are likely to increase with growing recognition of the disease and improved availability of serological testing. Yet, disease manifestations may occur after prodromal infections, particularly those caused by viral pathogens, such as influenza, Epstein—Barr virus, herpes simplex virus, and severe acute respiratory syndrome coronavirus 2 SARS-CoV-2 , to name a few [ 3 ]. Occasionally, patients with MOGAD have an overlap syndrome with anti-NMDA receptor encephalitis, characterized by clinical features of demyelination associated with encephalopathy, seizures, dyskinesias, or psychosis [ 5 ]. As the clinical spectrum of MOGAD continues to expand, so too does our appreciation for diagnostic and management challenges associated with this enigmatic condition. Key areas of ongoing research include determining the specificity and pathogenicity of MOG autoantibodies, identifying immunopathologic targets for future therapies, discovering and validating biomarkers that detect disease activity, and deciphering which patients with MOGAD require long-term immunotherapy.

Oji S, Nomura K. See "Optic neuritis: Pathophysiology, clinical features, and diagnosis", section on 'Optical coherence tomography'. Full criteria, along with supportive features and red flags, are listed above.

Myelin oligodendrocyte glycoprotein MOG is a glycoprotein believed to be important in the myelination of nerves in the central nervous system CNS. In humans this protein is encoded by the MOG gene. MOG's cDNA coding region in humans have been shown to be "highly homologous" [9] to rats, mice, and bovine, and hence highly conserved. This suggests "an important biological role for this protein". The gene for MOG, found on chromosome 6 p The crystal structure of myelin oligodendrocyte glycoprotein was determined by x-ray diffraction at a resolution of 1. This protein is residues long, and is a member of the immunoglobulin superfamily.

Federal government websites often end in. The site is secure. Myelin oligodendrocyte glycoprotein MOG -associated disease MOGAD is a rare, antibody-mediated inflammatory demyelinating disorder of the central nervous system CNS with various phenotypes starting from optic neuritis, via transverse myelitis to acute demyelinating encephalomyelitis ADEM and cortical encephalitis. Even though sometimes the clinical picture of this condition is similar to the presentation of neuromyelitis optica spectrum disorder NMOSD , most experts consider MOGAD as a distinct entity with different immune system pathology. MOG is a molecule detected on the outer membrane of myelin sheaths and expressed primarily within the brain, spinal cord and also the optic nerves. Its function is not fully understood but this glycoprotein may act as a cell surface receptor or cell adhesion molecule. The specific outmost location of myelin makes it a potential target for autoimmune antibodies and cell-mediated responses in demyelinating processes. Optic neuritis seems to be the most frequent presenting phenotype in adults and ADEM in children.

Myelin oligodendrocyte glycoprotein

Myelin oligodendrocyte glycoprotein MOG is a glycoprotein believed to be important in the myelination of nerves in the central nervous system CNS. In humans this protein is encoded by the MOG gene. MOG's cDNA coding region in humans have been shown to be "highly homologous" [9] to rats, mice, and bovine, and hence highly conserved. This suggests "an important biological role for this protein".

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Associated Data Data Availability Statement Data Availaiblity statement is not applicable as this review article is based exclusively on published work. J Clin Apher. No major sex differences have been found, and females and males appear to be much more equally affected compared with aquaporinIgG seropositive neuromyelitis optica spectrum disorder AQP4-IgG NMOSD , in which females predominate by a ratio of up to [ ]. Refer a Patient. Specifically, it is challenging to identify patients who will remain monophasic after their first attack. Unlike MS, neurological deterioration does not typically progress in the absence of relapses [ 5 ]. Corresponding author. It is important to exclude other potential causes. See 'MRI orbits' above. The latter is characterized by any combination of transverse myelitis and optic neuritis, sometimes with other CNS regions involved. Ann Neurol ;

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Key areas of ongoing research include determining the specificity and pathogenicity of MOG autoantibodies, identifying immunopathologic targets for future therapies, discovering and validating biomarkers that detect disease activity, and deciphering which patients with MOGAD require long-term immunotherapy. Ataxia and diplopia are the most common clinical accompaniments [ 22 ]. T2 hypointensity in the adjacent white matter has also been reported [ 45 ]. Language Chinese English. Transverse myelitis is reviewed here briefly and discussed in greater detail separately. Neurol—Neuroimmunol Neuroinflammation 7:e MOG encephalomyelitis: international recommendations on diagnosis and antibody testing. Once considered to be a severe form of MS targeting the optic nerves and spinal cord, NMOSD has since been recognized as a distinct autoimmune astrocytopathy with pathognomonic clinical features [ 2 , 6 ]. Female-to-male ratio is for AQP4-IgG seropositive cases Recurrent ON, myelitis, area postrema syndrome, cerebral syndromes, narcolepsy and diencephalic syndromes, acute brainstem syndromes. Neuromyelitis optica: evaluation of attacks and 1, treatment courses. MOG antibody disease affects males and females almost equally and are more prevalent in children than adults. International Business Collaborations. For this reason, a high degree of vigilance is needed to exclude alternative diagnoses.