Myelin oligodendrocyte glycoprotein (MOG) associated disease (MOGAD) is a rare antibody-mediated inflammatory demyelinating disorder of the central nervous system (CNS) characterized by a spectrum of phenotypes including optic neuritis (ON), acute demyelinating encephalomyelitis (ADEM), transverse myelitis (TM), and cortical encephalitis. Even though the clinical manifestations of MOGAD are similar to those of neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS), the widespread use of novel cell-based assays has enabled experts to recognize MOGAD as a distinct entity with different immunological pathogenesis. MOG is primarily expressed in the CNS and is located on the outer membrane of myelin sheaths. This glycoprotein's function is not fully understood; however, it may serve as a regulator of microtubular stability, cell surface receptor, or mediator of myelin fiber adhesion. Its position on the outermost surface of oligodendrocytes makes it an accessible target for autoantibodies that cause pathological alterations. Optic neuritis appears to be the most common initial manifestation in adults, whereas ADEM is most prevalent in children. The disease can either be monophasic or relapsing, the latter associated with ON as the initial assault, older age at onset, or persistence of MOG-Immunoglobulin-G (IgG) seropositivity. Despite this, demyelinating lesions on T2 MRI frequently remit, with secondary progression rarely linked to MOGAD, in contrast to MS, which typically has clinically silent residual, relapsing-remitting, and progressive lesions on MRI. Observational open-label experience indicates a need for high-dose intravenous (IV) steroids, (IV) immunoglobulins (IVIG), and plasma exchange in conjunction or alone in treating severe acute attacks. For maintenance therapy, chronic immunosuppressive medications, including oral steroids, oral immunosuppressants, and rituximab, are appropriate. Interestingly, MOGAD patients have more favorable outcomes than those with multiple sclerosis or aquaporin-4-IgG-NMOSD (AQP4-IgG-NMOSD), yet additional incident case studies are required to optimize treatments for relapse prevention.