![]() ![]() The other 80 percent of people behave very similarly clinically but don't have either of those biomarkers. For example, we know that only about 20 percent of people with recurrent episodes of optic neuritis have the MOG or the AQP4 antibody. What other antibody tests might become available? Many of these patients might have one or two optic neuritis attacks over five years and have normal visual outcomes. But whether all of these patients should be put on heavy-hitting immune suppression isn't 100 percent clear. The persistence of the MOG antibody might indicate a need for medication to prevent disease relapse and possibly reduce disability progression. In general, we would treat each attack, maybe aggressively, with steroids. This is a very interesting phenomenon and quite unusual in the field of autoimmune neurology. But if the antibody persists, the patient is at higher risk of another attack. Those patients are at low risk of another attack. Many of these patients will see a very rapid drop in MOG antibodies and test negative within six months. We've also found that the persistence of the MOG antibody is associated with disease relapses. We are planning a study to learn more about these phenotypes. The diseases are bizarrely different - AQP4 targets astrocytes while MOG targets oligodendrocytes - yet the phenotypes look quite similar. For example, in patients with recurrent optic neuritis, the visual outcomes are better with MOG-associated disease than AQP4-associated disease. It may actually indicate a more favorable prognosis. How does the presence of the MOG antibody affect disease course?
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