Experimental Multiple Sclerosis Drug May Repair Nerve Damage

Researchers find biological evidence of repaired myelin.

Researchers find biological evidence of repaired myelin.

An experimental drug for multiple sclerosis (MS) may be able to effectively treat nerve damage, according to a recent phase 2 study.

The study, presented at the American Academy of Neurology meeting in Washington, DC this month, indicates the drug may repair myelin, which provides protection to nerves and is damaged by MS.

"This study, for the first time, provides biological evidence of repair of damaged myelin in the human brain, and advances the field of neuro-reparative therapies," lead author Diego Cadavid, MD, said in a press release.

The study included 82 people who suffered from acute optic neuritis, a condition that affects just 1 eye and includes inflammation, nerve fiber damage, and myelin loss within the optic nerve. The study estimated approximately half of people with optic neuritis will go on to develop MS.

All of the patients received high dose steroids before being randomly selected to receive either the experimental antibody anti-LINGO-1 or a placebo once every 4 weeks for a total of 6 doses. The patients were assessed every 4 weeks for 6 months, with a final visit at 8 months.

The efficacy of anti-LINGO-1 in repairing myelin was evaluated through a comparison of optic nerve latency recovery in the damaged eye at 6 and 8 months with the other unaffected eye at the start of the study.

The study’s main finding focused on the latency of the visual evoked potential (VEP), which measures the ability of the visual system as a conductor of electrical signals between the retina and the brain. The researchers found that people treated with anti-LINGO-1 who did not miss more than 1 dose showed significantly improved conduction, measured by latency recovery, compared with people who in the placebo group.

At 6 months, patients who received the experimental drug improved by 7.55 milliseconds (34%) on average compared with placebo, which continued at 8 months with an average improvement of 9.13 milliseconds (41%) over placebo. Furthermore, the percentage of patients with VEP latency in the affected eye who recovered to normal or within 10% of the normal eye increased from 26% in the placebo group to 53% on anti-LINGO-1.

A substudy that utilized an exploratory method to measure latency called multifocal VEP showed similar effects from the treatment.

"More studies are needed to evaluate whether these changes lead to clinical improvement," Dr. Cadavid said.

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