In many kids, the MOG antibody disappears within 1 year, and relapses do not occur. 4Ĭhildren can be found to have the MOG antibody in the setting of ADEM however, a positive MOG antibody test in the setting of ADEM does not necessarily imply a course of MOGAD. Those with MOG antibody disease are more likely to have both optic nerves affected at the same time, and if the symptoms are in only one eye, the other optic nerve may show subclinical atrophy. Paraparesis (weakness) of a limb or limbs.Paralysis (no motor function) of a limb or limbs.Loss or blurring of vision in one or both eyes.MOG antibody disease preferentially causes inflammation in the optic nerve, 8 but can also cause inflammation in the spinal cord, brain, and brainstem.

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“But on its own, this antibody would probably not be sufficient in the case of MOGAD according to our research findings, because any therapy likely to succeed would also have to address the Fc receptors as a target structure,” says Mader. For a related condition (NMOSD with aquaporin-4 antibodies) a therapeutic antibody targeting a specific complement factor has been approved, which could potentially have some effect on MOGAD as well. There are currently no approved therapies for MOGAD. Where does it go from here? “The big goal would be to establish a treatment,” explains Mader. “The second pathomechanism of MOG antibodies, the enhanced activation of MOG-specific T cells, operates entirely via Fc receptors.” ´”We found that the destruction of the myelin sheath – that is, the insulating layer around nerves – is mediated by the complement system and by Fc receptor binding in roughly equal parts,” says Meinl. Next, the researchers tested selected antibody variants in an animal model. In vitro, these antibodies still recognized their target structure but differed in their ability to activate the complement system or bind Fc receptors. The researchers manufactured multiple variants of the humanized MOG antibody by means of mutagenesis. While the complement system plays an important role in the elimination of certain bacteria, it can also target the body’s own structures when things go wrong. The Fc fragment determines the biological effector functions, through binding to Fc receptors on immune system cells and through activation of the complement system. With their Fab fragment, antibodies recognize their specific target antigen. Antibodies consist of an antigen-binding fragment (Fab) and an Fc fragment. In a first step, the team led by Meinl and Mader humanized a monoclonal MOG antibody from established mouse models, equipping it with a human Fc fragment. Naoto Kawakami from University of Munich Hospital and further colleagues, including Professor Monika Bradl from the Medical University of Vienna, Meinl was able to demonstrate which effector mechanisms – that is to say, immunological responses – take place: Both the complement system and the binding of MOG antibodies to so-called Fc receptors on immune cells are involved in tissue destruction in patients with MOGAD, as the researchers report in the journal PNAS. “However, the MOG antibodies are not just diagnostic biomarkers, but play a decisive role in the disease process,” says Professor Edgar Meinl from LMU’s Institute of Clinical Neuroimmunology (Biomedical Center Munich) and University of Munich Hospital. Through idenfication of autoantibodies to MOG, neurologists are able to differentiate MOGAD and multiple sclerosis amongst others.

The disease progresses in bursts and there are no approved therapies. If the optic nerve is affected, it leads to vision defects, while inflammations of the spinal cord can cause paralysis. The autoimmune disease chiefly affects the optic nerve and spinal cord. Specific antibodies are directed against the so-called myelin oligodendrocyte glycoprotein (MOG), a protein on the outside of the insulating layer of nerve fibers. In this rare condition, the body’s defenses attack the myelin sheath, the outer layer of nerve fibers. MOG antibody-associated disease is an inflammatory autoimmune disease of the central nervous system, sharing some symptoms with multiple sclerosis (MS). Exploring the autoimmune disease MOGAD: Naoto Kawakami, Simone Mader, and Edgar Meinl (left to right).

Mog disease symptoms