Myelin oligodendrocyte glycoprotein

Skip to content. What is myelin oligodendrocyte glycoprotein antibody disease? Myelin oligodendrocyte glycoprotein MOG is a protein found on the covering of nerves in the central nervous system. While the precise function of MOG myelin oligodendrocyte glycoprotein not fully understood, it likely plays a role in myelin maturation, myelin integrity, and cell surface interactions.

Contributor Disclosures. Please read the Disclaimer at the end of this page. The disease has a predilection for children. Treatment and prognosis are reviewed separately. In a study using MOG self-antigen tetramers detected by a radioimmunoassay technique, MOG antibodies were detected in a subset of patients with acute disseminated encephalomyelitis ADEM but rarely in adult patients with MS [ 1 ].

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". 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. Also, MOG was shown to dimerize in solution, and the shape complementarity index is high at the dimer interface, suggesting a "biologically relevant MOG dimer. Developmentally, MOG is formed "very late on oligodendrocytes and the myelin sheath". Interest in MOG has centered on its role in demyelinating diseases. Some of them are not-inflammatory, such as adrenoleukodystrophy , vanishing white matter disease , and Rubella induced mental retardation. MOG has received much of its laboratory attention in studies dealing with MS. The proper way to identify it is by microarray, reacting patient serum with living cells, and detecting the binding IgG via a fluorescent-labeled secondary antibody. Anti-MOG antibodies have been shown to behave similarly to AQP4 antibodies in animal models, [20] and are considered a biomarker against the MS diagnosis [21] [22]. The presence of anti-MOG autoantibodies has been associated with the following conditions [27].

Am J Ophthalmol.

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. MOGAD causes painful swelling, known as inflammation.

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

Skip to content. What is myelin oligodendrocyte glycoprotein antibody disease? Myelin oligodendrocyte glycoprotein MOG is a protein found on the covering of nerves in the central nervous system. While the precise function of MOG is not fully understood, it likely plays a role in myelin maturation, myelin integrity, and cell surface interactions. MOG antibody disease affects males and females almost equally and are more prevalent in children than adults.

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The usual suspects for infectious bacterial, viral, and fungal encephalitis, paraneoplastic syndromes and other autoimmune encephalitis subtypes should be considered as part of the diagnostic evaluation. News Network. In vivo and in vitro studies suggest that MOG autoantibodies may cause primary demyelination in the CNS with loss of microtubule cytoskeleton in oligodendrocytes and altered expression of proteins [ 3 , 4 ]. Why UpToDate? Incidence and causes of overdiagnosis of optic neuritis. About this Site. The exact frequency of a monophasic course is not yet known with this newly identified disease, as longer follow-up is needed to better determine the relapse risk. A CD4-positive T cell inflammatory reaction with granulocytic inflammation is typical, which differs from MS, in which a CD8-positive predominant infiltrate is observed [ 6,7 ]. While the precise function of MOG is not fully understood, it likely plays a role in myelin maturation, myelin integrity, and cell surface interactions. Explore careers. Patients who show the symptoms listed above will undergo a serum blood test. Optical coherence tomography in acute optic neuritis: a population-based study. Sign up for free e-newsletters. Yet, it is worth mentioning that excluding patients with MOG IgG titers of without proper clinical analysis may lead to a significant number of missed diagnoses of MOGAD [ 33 — 35 ], further reiterating the need for thoughtful clinical judgment.

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.

See "Optic neuritis: Pathophysiology, clinical features, and diagnosis", section on 'Optical coherence tomography'. Admissions Requirements. Front Neurol In contrast to aquaporinIgG seropositive neuromyelitis optica spectrum disorder, the expression of aquaporin-4 is preserved in MOGAD, and astrocyte damage is much less prominent [ 6 ]. When bilateral it can be mistaken for papilledema [ 19 ]. Acta Neurol Scand. Brain MRI often shows normal findings or nonspecific white matter lesions. For this reason, it is reasonable to check for MOG-IgG in cases of suspected autoimmune or atypical encephalitis The usual suspects for infectious bacterial, viral, and fungal encephalitis, paraneoplastic syndromes and other autoimmune encephalitis subtypes should be considered as part of the diagnostic evaluation CLIPPERS MOGAD may rarely show a predilection for pontine involvement. Previously off label use of many agents was the mainstay of therapy, but targeted therapies approved for use in seropositive NMOSD include eculizumab, satralizumab, and inebilizumab. Supportive features — One or more of the following clinical and MRI features are required for the diagnosis in the absence of a clear positive cell-based serum MOG-IgG assay [ 37 ]:.