Myelin oligodendrocyte glycoprotein-associated disease (MOGAD) is a rare, antibody-mediated inflammatory disorder of the central nervous system (CNS) characterized by demyelination. It is caused by autoantibodies targeting myelin oligodendrocyte glycoprotein (MOG), a protein expressed on the surface of myelin sheaths. In MOGAD, acute inflammatory attacks occur when T cells and MOG-specific antibodies breach the blood-brain barrier (BBB), leading to targeted demyelination. Although its prevalence varies by region, MOGAD is generally less common than multiple sclerosis (MS). [1, 2].

The clinical presentation of MOGAD is diverse and can resemble other acquired demyelinating conditions, such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). It may present as monophasic or recurrent episodes of optic neuritis (ON), myelitis, brainstem syndromes, or acute disseminated encephalomyelitis (ADEM). Additionally, encephalitic symptoms, such as seizures, as well as cortical encephalitis and infratentorial syndromes, are recognized manifestations. [1,2].

The disease can follow either a monophasic or relapsing course. However, factors predicting relapse remain poorly understood, and data on the effectiveness of various immunotherapy regimens in preventing or reducing relapses are limited. Early recognition and accurate diagnosis of MOGAD are critical, as timely initiation of immunotherapy can significantly improve outcomes. [3].