Those with multiphasic disease – happening more than once – indeed remain on medications to avoid relapses. Therefore, not all patients with MOG have to be on immune-suppressing medications for their lifetimes. MOG patients tend to be younger than those with NMOSD, and the disease can be monophasic – happening only once – especially in children. Patients with MOG may experience optic neuritis - inflammation of the optic nerves, in which the protective myelin sheaths are damaged, and/or transverse myelitis - inflammation of a section of the spinal cord, in which the myelin is damaged. The biological function of MOG is not yet completely clear, but we know that it is a target of an aberrant immune response in people with this disorder.Īs one of a spectrum of opticospinal inflammatory disorders, MOG shares many characteristics with NMOSD. Of NMOSD patients who test negative for the aquaporin-4 antibody, approximately 40% have MOG antibodies.
Many labs around the world have adopted the protocol. The first article that proposed a protocol that reliably detects the MOG antibody was published in 2015. Glycoprotein – a type of protein molecule that has a carbohydrate attached to it.Oligodendrocyte – an abundant cell in the central nervous system that builds myelin.Myelin – protective sheath around nerves.But unlike NMO, which generally targets a water channel called aquaporin-4 on astrocytes, the immune dysfunction in MOG targets the myelin oligodendrocyte glycoprotein on the outermost myelin membranes surrounding the optic nerves, spinal cord and brain. Like NMO, MOG antibody disease is an autoimmune disease of the central nervous system (CNS). Now, MOG antibody disease is considered its own discrete diagnosis. In recent years, due to improvements in testing for MOG antibody in people, physicians can now distinguish those with MOG antibody disease from patients with multiple sclerosis or neuromyelitis optica. Myelin oligodendrocyte glycoprotein (MOG) is a myelin protein that has long been important in mouse models of demyelinating disease, causing loss or destruction of the protective sheath around nerves. Klawiter with a patient in the Neuromyelitis Optica Clinic Billing, Insurance & Financial Assistanceĭr.“The human myelin oligodendrocyte glycoprotein (MOG) gene: complete nucleotide sequence and structural characterization”. “Aquaporins and Their Regulation after Spinal Cord Injury”. Halsey, Andrea Conner, Alex Bill, Roslyn Logan, Ann Ahmed, Zubair (). Interpretation of the results must be made in the context of clinical signs and symptoms. Anti-MOG antibodies are NOT a reliable biomarker in adult onset multiple sclerosis. There is consensus that anti-MOG antibodies are important in both pediatric and adult demyelination, and the clinical association of MOG autoantibody-associated demyelination has been refined to include acute disseminated encephalomyelitis (ADEM), relapsing and bilateral optic neuritis, and transverse myelitis. MOG is also considered to serve a function as an adhesion molecule to provide structural integrity to the myelin sheath. MOG (Myelin oligodendrocyte glycoprotein) is a glycoprotein believed to be important in the myelination of nerves in the central nervous system. Autoantibodies against aquaporin-4 is prevalent in neuromyelitis optica (NMO). AQP4 facilitates water movement near cerebrospinal fluid and vasculature. Aquaporin-4 is one of the exclusive aquaporin proteins found in the central nervous system – particularly being the most prevalent aquaporin protein in the cerebellum and spinal cord grey matter.
Aquaporin-4, also known as AQP4 or NMO-IgG, is a water channel membrane protein that conducts water through the cell membrane.
Mitogen’s Neuromyelitis Spectrum assay is an autoimmune diagnostic test that detects autoantibodies to Aquaporin 4 & Anti-Myelin Oligodendrocyte Glycoproteins (MOG).
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