MOG antibody-associated disease (MOGAD)

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is a rare autoimmune inflammatory demyelinating disease.

MOGAD was described as a distinct entity in 2018 thanks to advances made in immunology techniques, allowing for the detection of antibodies against myelin oligodendrocyte glycoprotein (MOG), also known as “anti-MOG antibodies”, in the blood of patients with this disease. MOG is a protein found on the protective sheath of the nerves of the central nervous system (brain, spinal cord, optic nerve). When these antibodies attack the MOG protein, they cause inflammation.

What are the symptoms of MOGAD?

The most common manifestations are acute disseminated encephalomyelitis (ADEM, read more here), optic neuritis (read more here), transverse myelitis (read more here), encephalopathy with epileptic seizures, and brainstem involvement leading to balance, speech and swallowing disorders and double vision. The disease progresses with attacks, which can be severe. Treatment of the attack generally leads to a good recovery, although disability may persist in rare cases. MOGAD does not progress between attacks.

How is MOGAD diagnosed?

The diagnosis of MOGAD is established by clinical examination and the detection of anti-MOG antibodies, which are highly specific to this disease. This test is carried out at a reference laboratory. Complementary investigations, such as brain and spinal cord magnetic resonance imaging (MRI), lumbar puncture and blood sampling, help rule out other conditions that may be responsible for similar symptoms (differential diagnosis).

If anti-MOG antibodies disappear some time after the initial attack, this may lead to a diagnosis of monophasic disease (a single episode), especially when seen in children (read more about ADEM here), while their persistence may suggest a risk of relapse.

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