
Comment on our recent news article about a drug that might ultimately be useful for multiple sclerosis. Multiple sclerosis (MS) is the most common autoimmune disease of the nervous system. In an autoimmune disease, the body’s immune system malfunctions and attacks its own tissues. In MS, the immune system attacks and damages the layer of tissue (myelin) that covers nerve cells in the brain, spinal cord, and optic nerves (the nerves that send information from the eyes to the brain). If myelin is damaged or destroyed (demyelination), the nerve cells involved do not work properly. In people with MS, inflammation of the optic nerve (optic neuritis) causes loss of vision, pain with eye movement, and headache. Doctors use a test called visual evoked potential to measure the degree of optic nerve damage during an episode of optic neuritis. In the visual evoked potential test, doctors flash a light in the eye and measure the time it takes for the nerve impulse triggered by the light to reach the brain. In MS, demyelination causes the nerve impulse to be transmitted more slowly than normal.
All the currently available drugs for MS work by reducing inflammation and limiting further demyelination. The drugs do not repair damage that has already occurred. However, the study in the news article describes the first drug that is designed to repair damaged myelin. This new drug was shown to repair myelin in tests done in animals, so this was a preliminary study to see whether the drug would also repair myelin in people.
Doctors took 82 people with optic neuritis in one eye and gave some of them the new drug, called an anti-LINGO-1 antibody, and gave some of them an inactive substance (placebo). All the people also were given drugs to block inflammation. After 6 months of treatment, doctors did visual evoked potential tests. They found that in people who got the anti-LINGO-1 antibody, the nerve signal was transmitted 34% faster than in people given the placebo. They also found that nerve signal transmission recovered to normal or nearly normal in twice as many people who received the new drug (53% compared to 26%).
This is an important study because there currently is no drug that promotes remyelination in humans. The results are exciting but do not prove that the new drug should be used in people with MS. There are several reasons for caution:
However, this study is an encouraging first step that hopefully will be confirmed by additional tests.