MOGAntikörperErkrankungen

MOG antibodies are autoantibodies directed against myelin oligodendrocyte glycoprotein, a protein on the outer surface of myelin sheaths in the central nervous system. The antibodies are detected in serum using cell-based assays that present the native form of MOG. A positive MOG-IgG result helps distinguish MOG-associated disorders from multiple sclerosis and aquaporin-4–positive neuromyelitis optica spectrum disorders, though clinical overlap can occur.

The spectrum of MOG-IgG–associated disease (MOGAD) includes optic neuritis, acute disseminated encephalomyelitis (ADEM), transverse myelitis, or combinations of these events. In children, MOGAD frequently presents with ADEM-like features; in adults, optic neuritis and transverse myelitis are common. The clinical course can be monophasic or relapsing. Relapses are treated as attacks, and most patients have some degree of recovery, though residual deficits may occur after severe episodes.

Pathophysiology is thought to involve antibody-mediated demyelination, with MOG-IgG predominantly of the IgG1 subclass and potential involvement of complement activation. The disease shows distinct clinical and radiographic patterns compared with multiple sclerosis and AQP4-positive NMOSD, which aids differential diagnosis, but MRI findings can be variable across patients.

Diagnosis relies on a compatible clinical syndrome plus a positive MOG-IgG test in serum, with improved specificity achieved by use of live cell-based assays. Prognosis is generally more favorable than AQP4-positive NMOSD, especially in children, but relapses can occur. Treatment of acute attacks typically includes high-dose corticosteroids, with plasma exchange for steroid-refractory cases; longer-term immunotherapy may be considered in relapsing disease, using agents such as rituximab, mycophenolate, or azathioprine.