![]() 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.“If they judge the patient to have high relapse activity, a long-term relapse prevention strategy may be needed. “Clinicians should follow up with MOGAD patients for more than several years to judge the level of relapse activity in each case,” Dr. ![]() This, however, does not mean clinicians should stop monitoring these patients. “In MOGAD patients, however, indefinite long-term relapse prevention may be spared, especially in those with low relapse frequency and no neurological sequelae or only mild neurological sequelae.” “Patients with anti-AQP4-Ab may basically need long-term relapse prevention, because they surely experience much higher relapse activity, with much worse neurological disturbance,” Dr. Akaishi notes.Īs the investigators discussed, these findings demonstrate that long-term visual outcomes after optic neuritis are generally better in MOGAD patients than they are among those with anti-AQP4-positive NMOSD. “The titer level of serum anti-MOG-antibodies may not be useful to predict visual outcome,” Dr. These analyses found no significant differences between groups, which, they said, suggests that the titer level in the acute phase does not affect subsequent visual outcomes in these patients. Akaishi explains, “Whether IVMP therapy can improve the eventual visual outcome or not is uncertain, although our results suggest that IVMP administration during the acute phase would surely facilitate visual recovery.”įinally, the researchers examined the effect of serum disease-specific antibody titers on the visual prognosis of patients in the MOGAD and anti-AQP4 groups. However, the long-term benefits of such treatment in these patients are more ambiguous. The result? The best-corrected visual acuity at 5 years from the onset of optic neuritis among those who were treated with IVMP did not differ between patients in the MOGAD and MS groups ( P=.7481), but treatment did hasten visual recovery in the acute period. The study also assessed the efficacy of high-dose intravenous methylprednisolone pulse (IVMP) therapy with 1 to 3 cycles in the acute phase of optic neuritis. As part of the trial, they compared data from patients with MOGAD versus those with MS and anti-AQP4-positive NMOSD. The researchers evaluated the best-corrected visual acuity for each patient at nadir in the acute phase, as well as at 1 and 5 years from onset. All participants had been followed regularly for at least 5 years since the onset of optic neuritis. Akaishi and his colleagues enrolled 65 patients into the trial, 23 with MOGAD (31 involved eyes), 20 with MS (24 eyes), and 22 with anti-AQP4-positive NMOSD (24 eyes). Thus, although most clinicians have agreed that visual outcomes in MOGAD would be much better than that in AQP4-positive optic neuritis, it was not scientifically evidenced-based on data with a fixed disease duration.” “Consequently, disease duration in MOGAD patients in most previous studies was shorter than that in MS patients or AQP4-positive patients. “In addition, the disease concept of MOGAD has just emerged in the last decade,” he continues.
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