Scientists at the Sanford-Burnham Medical Research Institute have found a possible explanation for the loss of nerve function caused by multiple sclerosis and similar neurodegenerative diseases. The research provides a new approach to finding potential therapies.
A protein called contactin-1 is required to wrap nerves with myelin, a protective sheathing that enables proper function, the scientists found. When myelin is worn away, as in multiple sclerosis, nerves in the brain and spinal cord become damaged and don’t properly transmit sensory and motor signals.
Multiple sclerosis is considered an autoimmune disease, in which the body’s own immune system attacks the nerves for some unknown cause.
Contactin-1 acts like a messenger coordinating a construction crew. It directs myelin formation around axons, the long strands that carry impulses down nerve cells, said Barbara Ranscht, who led the research. Without the protein, myelin-producing cells called oligodendrocytes don’t do their jobs.
Working in mice, the researchers found the protein was produced in both the oligodendrocytes and the axons during myelination.
The researchers also inactivated the gene for making contactin-1 in mice. The offspring died shortly after birth, displaying a greatly reduced production of myelin. Moreover, what myelin was produced wasn’t functional, because it wasn’t attached to the axons, Ranscht said.
Myelin formation takes many steps that must be performed in harmony, Ranscht said.
“First of all, the axons need to be there, then the oligodendrocytes come to the axons. They proliferate, they make more cells, then the cells align nicely along the axons, then they get signals from the axons to make the myelin,” she said. “The axons get signals from the oligodendrocytes to be myelinated. It’s a constant cross-talk between the two different cells. What we show in the paper is that contactin is absolutely necessary for this cross-talk.”
Although the study was performed in animals, there’s evidence of the protein’s role in people. A 2011 paper in PNAS found that contactin-1 is involved in development of precursor cells to the myelin-forming oligodendrocytes. Moreover, a 2009 study also in PNAS found that a related molecule called contactin-2 is targeted in an autoimmune response in multiple sclerosis patients.
The study is impressive, said P. Hemachandra Reddy, a neuroscientist at Oregon Science & Health University who published his own research on multiple sclerosis Dec. 26. Reddy and colleagues found that an antioxidant called MitoQ reverses symptoms in mice with an MS-like demyelinating disease.
“This is a very well-executed study,” Reddy said. “I am excited to see this paper.”
The paper described the function of contactin-1 in the optic nerve, providing an explanation for why multiple sclerosis patients may experience blurred vision, Reddy said.
“We did not look at the contactin protein levels in our study; we are going to look at it now, because it makes a lot of sense,” he said. “Maybe MitoQ is enhancing contactin levels.”
Ranscht emphasized that the Sanford-Burnham study represented basic research, and years of further work would be needed before any potential drug could be found. But on the positive side, the research provides a clear guide about what to look for, namely a drug that restores contactin functioning.
“This is something that is a top priority on our research list. ... Is this really the molecule that might help to restore myelin in a demyelinating disease?” Ranscht said. “It’s exciting, because we have a candidate now to look for. That’s where we are. We don’t have a cure.”
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