The Pathophysiology of Myelin Oligodendrocyte Glycoprotein Antibody Disease
Myelin oligodendrocyte glycoprotein (MOG) antibody disease is an important disease to understand, potentially causing devastating disability in children, including infants, as well as adults by attacking the eyes, brain and spinal cord. It can leave people blind, immobile and with impaired cognition. It has similarities with multiple sclerosis, with both diseases targeting "myelin", the insulation covering nerve fibres, causing "demyelination". MOG antibody disease (MOGAD) is the commonest cause of acute demyelination in children.
MOGAD is diagnosed when people develop neurological disease with MOG antibodies in their blood. Antibodies are produced in healthy people to fight infections. In MOGAD, antibodies are erroneously produced against MOG, a protein found on myelin. It is unclear whether these antibodies cause demyelination in MOGAD. The function of MOG is currently unknown, but there is some evidence suggesting it may play an important role in "autoimmune" diseases in the brain, where the body’s own defence system attacks the brain by mistake.
My research will focus on answering two questions using a cellular and mouse model of MOGAD:
(1) Does MOG interact with an immune cell in the brain, called "microglia"
(2) Do antibodies found against MOG in patients with MOGAD cause disease?
Understanding this may help us to find better treatments for MOGAD and other similar diseases like multiple sclerosis.