Study details method for testing recovery from multiple sclerosis

A new study from UW-Madison researchers details a method for testing recovery from multiple sclerosis. 

In multiple sclerosis — or MS — the body’s immune system causes inflammation that damages nerve fibers as well as myelin, an insulating fatty substance supporting nerve function. MS also harms the cells responsible for creating myelin. 

Successful treatments exist for certain patients with MS, according to Ian Duncan, a neuroscientist at UW-Madison’s School of Veterinary Medicine. But he says others experience more advanced forms of the disease that result in a steeper decline. 

“There are no effective treatments for them,” he said. 

But that could change as drug development companies work to create restorative treatments for myelin loss. As this insulating material is regrown, healthy nerve function can be restored. 

In patients being treated for MS, physicians will often monitor functionality with a test called the visual evoked potential. By shining lights into victims’ eyes and monitoring the delay in related brain activity, doctors can observe the effects of the disease. 

“When that latency increases, it’s taking longer for the signal from the lights to get from the retina down the optic nerve to the brain,” Duncan said. “As MS progresses and demyelination of axons in the optic nerve worsens, the latency grows because the axons are not conducting the signal as well as healthy nerves.”

In a study published last month, Duncan and other researchers connected changes in latency during the VEP test to myelination of nerves. 

“You’ve got a way to tell if there’s improvement in a patient — an outcome measure that can show whether the drug you are testing is successfully promoting myelin repair,” he said. 

The research team used feline animal models for the study. By feeding them irradiated food over a period of several months, they induced severe myelin loss in the cats’ nervous systems including their optic nerves. Researchers measured nerve signal latency before the demyelination, during the symptoms, and after the animals recovered. 

Nerve function was restored in the test animals once their diets returned to normal. 

“The normal latency of the VEP in the cats is between 50 and 60 milliseconds. At the height of the disease, it goes up to 90 to 110 milliseconds,” Duncan said. “And then, at recovery, it comes back down to around 60 to 70 milliseconds.” 

Scientists also took tissue samples from the cats that showed their nerves regained myelin as the test latency times decreased. Duncan explains latency didn’t “fully recover,” because the regrown myelin is thinner than the myelin that was lost. 

Still, he says previous studies have shown that thin myelin “is enough to restore function and sufficient to protect nerve fibers in the long run.”

According to Duncan, the study identified a “proven outcome measure” for drugs aimed at repairing myelin in patients with MS. Because the remyelinating effect in the optic nerve reflects a similar change throughout the central nervous system, he says this understanding “can help begin to sort the wheat from the chaff in potential remyelinating therapies for people with progressive MS.”