Scientists at the Tohoku University reported in Asia Research News that antibodies are responsible for the difference between various disorders and multiple sclerosis (MS). These disorders affect the myelin sheath surrounding nerve fibers.
Their findings indicate that certain ‘inflammatory demyelinating disorders’ should be categorized differently and not as multiple sclerosis. They should also be treated in accordance with their specific disease mechanism.
About Myelination
Myelination is the process of forming the myelin sheath that surrounds a nerve. This allows nerve impulses to move.
About Demyelination
Demyelinating diseases are conditions that damage the protective cover (myelin sheath) surrounding nerve fibers in the brain, optic nerves, or spinal cord. Damage to the myelin sheath causes nerve impulses to slow or shut down. This will cause various neurological symptoms.
MS is perhaps the most common demyelinating disorder of the central nervous system (CNS). Inflammation and the resulting injury to the myelin sheath may result in sclerosis (scarring).
A New Approach to Diagnosing MS
The scientists discovered that some patients who have demyelinating disorders accompanied by inflammation have autoimmune antibodies that act against the glycoprotein MOG. This glycoprotein is deemed to be critical in the maintenance of the structural integrity of the myelin sheath.
MOG is involved in the central nervous system autoimmunity in two ways.
- MOG-specific T Cells can cause inflammation in the central nervous system
- Anti-MOG antibodies cause damage to the myelin sheath (demyelination)
MOG is rarely found in MS patients. However, it is found in patients with optic neuritis, myelitis, and other disorders.
The Tohoku University scientists analyzed lesions in the brains of patients with inflammatory demyelinating disease who had MOG antibodies. They also analyzed lesions in patients who did not present with the antibodies. The scientists discovered a significant difference between the two.
When the scientists autopsied brain lesions of people who had been diagnosed with MS and neuromyelitis optica spectrum disorder (NMOSD), they did not find MOG antibodies.
A Different Story
Lesions from NMOSD patients uncovered reductions in astrocytes (nerve cells) and oligodendrocytes (myelin-producing cells) as well as a loss of internal layers of proteins in the myelin sheath.
A different story emerged with biopsies from patients with MOG antibodies who had been diagnosed with other inflammatory demyelinating diseases.
These patients showed rapid demyelination in lesions surrounding small veins. Notably, there was a deficiency of the MOG protein in myelin sheaths. This was an indication that the MOG protein was damaged by attacks from MOG antibodies.
When comparing MS and NMOSD lesions to oligodendrocytes, the latter was mostly preserved.
The scientists summarized their findings by stating that MOG antibody-associated disorders are in a different autoimmune demyelinating disease category than MS and NMOSD.
They recommend that in the future, therapeutic strategies should be individualized when examining patients with inflammatory demyelinating disorders in accordance with the specific demyelinating mechanism.
