A new study published online in Nature Neuroscience has again raised an important possibility about how MS develops. Examining a mouse model of MS, the researchers used a specific toxin to destroy the cells that produce myelin in the central nervous system, the oligodendrocytes.
Initially, the mice recover from the damage to these myelin-producing cells, which start to produce myelin again and re-myelinate the nerve cells. But then at about 40 weeks after the toxin is administered, the mice develop progressive neurological deterioration and die. This is shown to be due to inflammation that is triggered by the initial process of myelin breakdown. So inflammation may not be at the heart of the disease process in MS, but may be a secondary phenomenon to the initial damage to myelin.
This is not the first time it has been suggested that inflammation is a secondary phenomenon in MS causation. It may explain why immunomodulatory therapies are only partially effective in modifying the disease, and not really effective at all once the progressive phase of the disease has been reached.
It also emphasises the importance of developing therapies and techniques that assist remyelination and myelin repair, particularly early in the disease course. This mouse model may prove to be quite helpful in studying new therapies for MS.