Multiple sclerosis (MS) is a disorder that causes the immune system to attack the central nervous system. It’s considered to be an immune-mediated disorder rather than autoimmune disorder. This is because it’s not known exactly what substance the body’s immune cells are targeting when they begin to go into attack mode. Experts think environmental factors might trigger MS in people who are genetically susceptible to the disorder.
The immune system begins attacking myelin inside the central nervous system. Myelin is a fatty substance that coats the nerve fibers of the brain and spinal cord. It insulates the nerves and helps speed the conduction of electrical impulses along the spinal cord to and from the brain. Once the immune system begins its attack, it eats away at this myelin coating. This disrupts the signals from the brain to the rest of the body.
Your five senses, muscle control, and thought processes depend on the transmission of nerve signals. When MS disrupts these pathways, multiple symptoms can occur. Depending on the site of the damage, a person with MS can experience numbness, paralysis, or cognitive impairment. Common symptoms include pain, a loss of vision, or trouble with bowel and bladder function.
Usually, a person with MS experiences one of four disease stages called courses, which include the following:
- Clinically isolated syndrome (CIS) is the least severe course of MS, and it shares some milder characteristics with MS but is not technically MS. People who have CIS may or may develop MS.
- Relapsing-remitting MS (RRMS) is the most common MS disease course. It’s characterized by new or increasing neurological symptoms of disease, sometimes with relapses and remissions.
- Primary progressive MS (PPMS) is more severe than RRMS and is characterized by worsened neurological function without relapses or remissions
- Secondary progressive MS (SPMS) follows a relapsing-remitting course of MS, meaning that most people diagnosed with RRMS develop SPMS.
Stopping or slowing the immune system from attacking myelin has been the main goal of MS therapies since the first treatment came on the market in 1993. All of the FDA-approved drugs are designed to slow the rate of relapse and the accumulation of disability. None of them can undo the scarring that occurs due to MS. If the damage to myelin is severe enough, the disability can become permanent.
The body tries to repair the damage on its own using cells called oligodendrocytes to regrow the myelin. Early on in the disease, the repair process can restore most, if not all, nerve function. However, it becomes less efficient over time, and disability mounts.
So why does this myelin regeneration process eventually fail in MS? According to researchers at Weill Cornell Medical College, the body relies on a balance of on and off signals in biological processes like remyelination. In MS, researchers believe off signals inhibit the repair of myelin. Off signals warn your body that the environment is too hostile for growth. Inflammatory processes at work in MS cause these warning signals.
The goal of much of MS research is to figure out how to repair myelin and restore function. Remyelination could effectively reverse disability once thought to be permanent. Scientists all over the world are working toward this goal.
Researchers at Case Western Reserve School of Medicine have recently discovered how to turn ordinary skin cells into oligodendrocytes. These are cells that can regrow myelin and reverse damage that occurs due to diseases such as MS. In a process known as “cellular reprogramming,” researchers retrained the proteins in skin cells to become precursors to oligodendrocyte cells. The research team was able to quickly grow billions of these cells. This discovery will help scientists turn a readily abundant cell into a building block for myelin regrowth.
Recently, a new drug called fingolimod (Gilenya) has been approved for people with RRMS. It works by preventing neuro-inflammation, but it also appears to be able to help people by directly enhancing nerve regeneration and remyelination. It works by inhibiting the action of a certain enzyme that creates a fatty acid that damages myelin. One study showed that Fingolimod could promote nerve regeneration, reduce nerve inflammation, and improve myelin thickness.
Other efforts to regrow myelin are also underway. Researchers in Germany are in the early stages of experimenting with human growth hormone to encourage production of myelin. Their initial results are promising, but more studies are necessary.
Research in MS remyelination is on the brink of exciting breakthroughs. Scientists from around the globe are focusing their efforts on new ways to solve this problem. Some are trying to control the inflammatory processes and turn off switches back on. Others are reprogramming cells to become oligodendrocytes. These efforts bring scientists one step closer to helping people with MS. For example, regenerating the nerve’s myelin covering may allow people with MS who can’t walk to walk again.