MOG (myelin oligodendrocyte glycoprotein) antibody disease (MOGAD) or MOG antibody-associated encephalomyelitis (MOG-EM) is an inflammatory demyelinating disease of the central nervous system. Serum anti-myelin oligodendrocyte glycoprotein antibodies are present in up to half of patients with an acquired demyelinating syndrome and have been described in association with a range of phenotypic presentations, including acute disseminated encephalomyelitis, optic neuritis, transverse myelitis, and neuromyelitis optica.

The clinical presentation is variable and largely dependent upon the overall clinical manifestation.^{[citation needed]}

The presence of anti-MOG autoantibodies has been described in association with the following conditions:

The most common presenting phenotypes are acute disseminated encephalomyelitis (ADEM) in children and optic neuritis (ON) in adults. Some of these phenotypes have been studied in detail:

Anti-MOG antibodies have been described in some patients with NMOSD who were negative for the aquaporin 4 (AQP-4) antibody. However, most NMOSD is an astrocytopathy, specifically an AQP4 antibody-associated disease, whereas MOG antibody-associated disease is an oligodendrocytopathy, suggesting that these are two separate pathologic entities. Rare cases have been described of patients with antibodies against both AQP4 and MOG. These patients typically have MS-like brain lesions, multifocal spine lesions and optic nerve atrophy. However, the coexistence of both antibodies is still a matter of ongoing debate.

The presence of anti-MOG antibodies is more common in children with ADEM.

Rare cases of anti-MOG antibodies in association with tumefactive multiple sclerosis have been described.

The reason why anti-MOG auto-antibodies appear remains unknown.