Should We test for IgG Antibodies Against MOG in Both Serum and CSF in Patients With Suspected MOGAD?

Myelin oligodendrocyte glycoprotein (MOG), a transmembrane protein expressed on the surface of oligodendrocytes and the outermost surface of myelin sheaths, was once considered a potential antibody biomarker of multiple sclerosis (MS).¹ However, the development of more reliable and specific cell-based assays (CBAs) to detect serum immunoglobulin G autoantibodies against MOG (MOG-IgG) and their increasing availability has enabled us to recognize that they are the hallmark of a distinct disease within the inflammatory demyelinating spectrum of the CNS).² This condition is now known as MOG antibody–associated disease (MOGAD).³ The typical phenotypes of MOGAD include optic neuritis, acute disseminated encephalomyelitis, transverse myelitis, and, less commonly, cerebral cortical encephalitis or other brain manifestations, either alone or in combination.³ Initially, MOGAD was considered a subset of neuromyelitis optica spectrum disorder (NMOSD) because MOG-IgG was detected in many patients fulfilling the diagnosis for aquaporin-4–IgG (AQP4-IgG) seronegative NMOSD. However, it is important to exclude MOGAD when diagnosing NMOSD. Despite some overlapping features, there are clinical, radiologic, and pathologic findings that distinguish MOGAD from MS and AQP4-IgG seropositive NMOSD.³ Given the therapeutic and prognostic differences between these diseases, an accurate and timely diagnosis is of utmost importance.