Doctor and patient
Dr. Klawiter with a patient in the Neuromyelitis Optica Clinic

Myelin oligodendrocyte glycoprotein (MOG) is a myelin protein that has long been important in mouse models of demyelinating disease, causing loss or destruction of the protective sheath around nerves. In recent years, due to improvements in testing for MOG antibody in people, physicians can now distinguish those with MOG antibody disease from patients with multiple sclerosis or neuromyelitis optica. Now, MOG antibody disease is considered its own discrete diagnosis. Like NMO, MOG antibody disease is an autoimmune disease of the central nervous system (CNS). But unlike NMO, which generally targets a water channel called aquaporin-4 on astrocytes, the immune dysfunction in MOG targets the myelin oligodendrocyte glycoprotein on the outermost myelin membranes surrounding the optic nerves, spinal cord and brain.

What is MOG? 

  • Myelin – protective sheath around nerves
  • Oligodendrocyte – an abundant cell in the central nervous system that builds myelin
  • Glycoprotein – a type of protein molecule that has a carbohydrate attached to it

The first article that proposed a protocol that reliably detects the MOG antibody was published in 2015.  Many labs around the world have adopted the protocol. Of NMOSD patients who test negative for the aquaporin-4 antibody, approximately 40% have MOG antibodies. The biological function of MOG is not yet completely clear, but we know that it is a target of an aberrant immune response in people with this disorder.

As one of a spectrum of opticospinal inflammatory disorders, MOG shares many characteristics with NMOSD. Patients with MOG may experience optic neuritis - inflammation of the optic nerves, in which the protective myelin sheaths are damaged, and/or transverse myelitis - inflammation of a section of the spinal cord, in which the myelin is damaged.

MOG patients tend to be younger than those with NMOSD, and the disease can be monophasic – happening only once – especially in children. Therefore, not all patients with MOG have to be on immune-suppressing medications for their lifetimes. Those with multiphasic disease – happening more than once – indeed remain on medications to avoid relapses.  MOG strikes males and females equally. More people with MOG suffer with optic neuritis than with transverse myelitis. Simultaneous optic neuritis of both optic nerves occurring at the same time is a characteristic feature of MOG antibody disease.

MOG antibodies have been detected in a number of other rare CNS disorders. Among children, one common presentation of MOG antibody disease is acute disseminated encephalomyelitis (ADEM) in which inflammation occurs in the brain, as well as the spinal cord and optic nerves. ADEM generally follows an infection and causes a single episode only. Less commonly, MOG may be revealed as AFP (acute flaccid paralysis) which causes sudden weakness and even paralysis. MOG antibodies are also commonly found in adults with CRION (chronic relapsing inflammatory optic neuropathy).

There are currently no FDA-approved medications for those with MOG antibody disease. The NMO Clinic and Research Lab is pleased to be conducting both an animal study and a clinical trial for a potential drug for this disorder.