As it has become apparent that there are differences in MOG epitope binding between species, translation of animal studies to human demyelination should be analyzed in this context. It is imperative to understand whether anti-MOG antibodies are indeed pathogenic, and if so, their mechanisms of action. Patients with MOG antibody-associated demyelination appear to have a unique clinical, radiological, and therapeutic profile, which represents a major advance in their diagnosis and management. Anti-MOG antibodies are now thought not to be associated with multiple sclerosis in adults. Immunologically, there is an array of circulating serum auto-antibodies and pro- and anti-coagulant proteins that may occur in a highly variable pattern. Anti-myelin oligodendrocyte glycoprotein antibodies (MOG-ab) are associated with acute disseminated encephalomyelitis (ADEM), neuromyelitis optica spectrum. There is now international consensus that anti-MOG antibodies are important in both pediatric and adult demyelination, and the clinical association of MOG antibody-associated demyelination has been refined to include acute disseminated encephalomyelitis, relapsing and bilateral optic neuritis, and transverse myelitis. However, the relevance of anti-MOG antibodies in humans has been difficult to decipher over the years due to varying methods of detection as well as the fact that it was assumed that these antibodies would be clinically associated with multiple sclerosis. Seminal studies using murine anti-MOG antibodies have highlighted the fact that antibodies that target epitopes of native MOG in its conformational state, rather than linearized or denature`d MOG, are biologically relevant. He was diagnosed with MOG-IgG-associated encephalitis and treated with antiepileptic drugs (levetiracetam) and intravenous pulse methylprednisolone (500 mg/day for 3 days), followed by oral prednisone (60 mg qd) and mycophenolate mofetil (0.5 g bid) induction. MOG has been identified as a putative candidate autoantigen and autoantibody target in demyelination for almost three decades, with extensive literature validating its role in murine models of experimental autoimmune encephalomyelitis. Objective To describe the presentations, radiologic features, and outcomes of children with autoimmune encephalitis associated with myelin oligodendrocyte glycoprotein antibodies (MOG abs). However, a CBA revealed anti-MOG-IgG in his serum (1:100).

Myelin oligodendrocyte glycoprotein (MOG) is a protein exclusively expressed on the surface of oligodendrocytes and myelin in the central nervous system.

Anti mog encephalomyelitis