As researchers continue to study disorders like neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS), we are learning more and more about factors that contribute to the disease processes seen in these conditions. For example, demyelination from MS is thought to be caused by the activation of white blood cells called T cells (and maybe B cells), while most cases of NMOSD involve antibodies to aquaporin-4 (anti-AQP4 or NMO-IgG). There has recently been more discussion about Myelin Oligodendrocyte Glycoprotein or MOG, and its relationship to NMOSD. Although MOG’s exact function is not fully known, it is thought to be an important glycoprotein that influences the myelination of nerves in the central nervous system. Anti-MOG antibodies have been found in individuals diagnosed with NMOSD who do not have antibodies to AQP4, in acute disseminated encephalomyelitis, transverse myelitis, and optic neuritis. Those with anti-MOG NMOSD tend to have attacks most often in the optic nerve, or optic neuritis (ON), but can also present with inflammation in the spinal cord (transverse myelitis) and brainstem.
Recently at The European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) annual meeting, there was a discussion about anti-MOG and whether it should be its own diagnostic category or another variant of NMOSD. Dr. Douglas Sato of the Brain Institute of the Rio Grande do Sul in Porte Allegre, Brazil, argued that there are enough differences between anti-MOG disease and NMOSD, and proposed that it be called MONEM, an acronym for “anti-MOG associated optic neuritis, encephalitis and myelitis (MONEM).” In contrast, Dr. Roman Marignier of the Hospital Pierre Wertheimer of Lyon University Hospital in France argued that anti-MOG disease is a variant of NMOSD that occurs without antibodies to AQP4. His argument was that patients with anti-MOG and patients with anti-AQP4 disease have similar cerebrospinal fluid characteristics, clinical characteristics, MRI characteristics, and the same acute and long-term treatment options.
Another presentation at ECTRIMS described a study that followed 33 children and 26 adults who were anti-MOG-positive over an average of five years. Researchers from the Kids Research Institute at the Children’s Hospital at Westmead in Sydney, Australia, found that 54% of all patients developed optic neuritis as their first disease sign. They found that the individuals in the study responded well to steroids, but relapsed when steroids were stopped. They found that their study participants had reduced relapse rates when they were on maintenance steroids, intravenous immunoglobulin (IVIg), or immunosuppression with rituximab or mycophenolate.
Participate in Research on anti-MOG
Dr. Michael Levy and the NMO lab at Johns Hopkins University are developing tests for Anti-MOG (myelin oligodendrocyte glycoprotein) disease. They are especially looking for participants with recurrent clinical events of optic neuritis and/or transverse myelitis with either a negative anti-AQP4 antibody test or a positive anti-MOG antibody test from another lab.