A pair of scientists at the Oklahoma Medical Research Foundation are bringing together their expertise to find new ways to study one of the most prominent symptoms of multiple sclerosis: vision loss.
MS is an autoimmune disease where the body’s immune system attacks its own healthy tissues. The disease attacks myelin, the protective layer that covers nerves and fibers throughout the body. This damages the nervous system’s ability to carry signals to and from the brain, causing a wide range of symptoms that include problems with vision, tremors, paralysis, muscle spasms and more.
For nearly 20 percent of MS patients, vision loss is the first symptom of the disease and often occurs long before an MS diagnosis. This vision loss, called optic neuritis, occurs when the myelin protecting the optic nerve is stripped away, resulting in temporary blindness. This usually occurs in one eye.
“It just happens out of the blue,” said OMRF vision researcher Scott Plafker, Ph.D. “The optic nerve transmits information from your retina to your brain, telling your brain that your eye has seen an image, and your brain then interprets that image and processes it. When that nerve becomes inflamed, that process is interrupted and you lose your vision.”
At some point, more than 50 percent of all MS patients will experience optic neuritis. MS flares cause worsening of this vision loss, but when they resolve, the vision usually comes back. In some cases, though, repeated instances of vision loss can become permanent.
Plafker and OMRF MS researcher Bob Axtell, Ph.D., teamed up to look at how they can help cells in the eye better protect themselves and prevent long-term loss of eyesight in MS.
Their research, published in the scientific journal Molecular Vision, revealed that mouse models of optic neuritis showed the same flaring processes that human patients experience. The vision wanes and then recovers in a cycle, which had never been shown before in mice.
The OMRF researchers also determined that a loss of specific cells, called retinal ganglion cells, occurs in a particular pattern, indicating that central vision is especially vulnerable to these disease flare-ups.
“Through this research, we found there are two different immune pathways that can drive the inflammation in the central nervous system,” said Plafker.
Axtell added, “These pathways determine how bad the optic nerve damage is, and that’s what we’re seeing in this research. We’ve observed this phenomenon in mice before, but now we’re seeing what’s actually going on in greater detail. It’s very exciting.”
Now that they know the pathways associated with the strength of the disease, researchers can use them as specific targets for therapy. With the discovery that mice serve as a reliable model for optic neuritis, Plafker said they can monitor inflammation in the optic nerve and loss of cells, as well as responses to treatments or other factors.
“We’re trying to protect the nerve, which is your eye’s ability to communicate to the brain,” said Plafker. “When that communication channel is disrupted or damaged, vision loss occurs.”
Chelsea Larabee in the Plafker laboratory spearheaded the project with assistance from OMRF researchers Jonathan Wren, Ph.D., Shruti Desai, Yang Hu, Constantin Georgescu, Ph.D.
This work was supported by a Nathan Shock Center Grant, number P30AG050911, from the National Institutes of Health.
