UPDATED: Myelin damage doesn't bring on MS, researchers find

Damaged myelin doesn't trigger multiple sclerosis, scientists at the University of Zurich and elsewhere have found, discrediting a long-held theory about the deadly disease.

Many have believed that the death of cells known as oligodendrocytes, which produce the myelin sheath in the brain and spinal cord, triggers the neuromuscular disease that leads to a loss of muscular control, vision, balance and sensation, without significant immune system involvement. The disease itself has long been known to be an autoimmune condition, where the body's defenses attack the myelin. What's at issue here is determining the actual trigger that brings on the disease in the first place.

This group of scientists now asserts that that theory no longer has any standing. To come to this conclusion, they explain that they induced myelin defects in mice without triggering their autoimmune system, and no MS-autoimmune disease cropped up. Subsequent tests focused on myelin damage and triggering an autoimmune response, but as before, the mice didn't develop anything resembling MS, the researchers noted in their announcement of the study findings.

This discovery is a small step, in some ways. But part of finding out what causes a disease, and hopefully how to cure it, is to rule out (or prove) long-standing beliefs and theories about what brought on the disease in the first place. The researchers say their finding will help push future research into what triggers MS away from the brain, and closer to the immune system. So if their own finding holds, they've taken one crucial step forward in MS research, looking beyond drugs already on the market from Biogen Idec ($BIIB) and others that help manage the disease but don't cure it.

Further details of the finding are published in Nature Neuroscience.

(Editor's Note: This article updates an earlier version that lacked mention of the researchers' finding as part of a full study, as well as the study's place of publication.)

- here's the release
- read the journal abstract

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