Myelin oligodendrocyte glycoprotein (MOG) is a protein involved in the maintenance of the myelin structure. Recent studies have shown that serum anti-MOG antibodies are found in some of the patients who meet the diagnostic criteria for neuromyelitis optica spectrum disorders, but do not have detectable aquaporin-4 (AQP4) antibodies. Anti-MOG antibodies are components of the inflammatory response to myelin leading to primary demyelination, while the anti-AQP4 antibodies mediate astrocyte destruction in the first place. The available data on the diverse immunopathological mechanisms, demographic characteristics of patients as well as the clinical course suggest the need for classifying anti-MOG-related disorders as a separate form of demyelinating disease. The clinical picture is dominated by an isolated optic neuritis, which is bilateral in 50% of cases. Myelitis and encephalitis are less common manifestations. Long-term prognosis should be considered serious. Long-term disability, mainly in the form of reduced visual acuity and unsteady gait, is observed in almost half of patients. Previous studies showed that intravenous corticosteroid therapy is most effective for relapses, while therapeutic plasma exchange should be used if the desired clinical effect is not observed. As for maintenance therapy, most data support the use of corticosteroids. Reports on relapse prevention using intravenous immunoglobulin preparations, rituximab and other immunosuppressants are also available. The knowledge on MOG antibody-associated neurological conditions is certainly incomplete. Further systematic research is needed, particularly in the context of effective differentiation with other demyelinating conditions and efficacious therapy.