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Multiple Sclerosis (MS) is a condition where the immune system attacks and destroys myelin: the protective coating of nerve fibers, which triggers movement problems characteristic of the disease. Researchers are now suggesting that they may have discovered a way to restore myelin formation, bringing ever closer the possibility of new treatments for MS.

In their new study, lead investigator Richard Lu, Ph.D., of the Brain Tumor Center at Cincinnati Children’s Hospital, and his colleagues have recently reported that microRNA (called miR-219) reactivated myelin-producing cells in mouse models of multiple sclerosis which then restored their limb function.

According to the National Multiple Sclerosis Society, approximately 2.3 million people worldwide are living with MS. If a person is diagnosed with MS, their immune system attacks myelin, which is a fatty substance that protects nerve fibers in the central nervous system (CNS), as well as the cells that produce myelin, known as oligodendrocytes. This damages the nerve fibers, which then stops them from transmitting signals between the brain and spinal cord. Consequently, this is how neurological symptoms such as numbness, muscle weakness, walking difficulties or tingling in the face, body or other extremities can occur as a result.

Researchers have been increasingly investigating ways to stimulate oligodendrocyte function as part of trying to restore myelin in patients with MS. Lu and his colleagues are seeking to reveal how the microRNA miR-219 might just able to accomplish that.

MicroRNAs are fragments of RNA found on cell chromosomes which aid in regulating gene expression. In some cases, micoRNAs have been known to inhibit the activity of genes within cells. In previous studies, damaged nerves and tissues of patients with MS and other neurodegenerative diseases were shown to be lacking in miR-219. With this mind, Lu and his team hypothesized that miR-219 might be the key to helping protect against nerve damage.

In the study, the researchers erased miR-219 in mice models of MS and studied the effects. The mice then had MS-like myelin damage triggered by the autoimmune disorder encephalomyelitis, and a subsequent exposure to the chemical compound lysolecithin. The researchers found that the lack of miR-219 activated several proteins involved in preventing myelin formation, including a protein called Lingo1. Upon further study, the researchers found that miR-219 creates part of a network which inhibits the myelin-producing function of oligodendrocytes.

Following this, Lu and his team wanted to determine whether miR-219 would possibly be able to stimulate oligodendrocyte activity, and did so using a synthetic version of miR-219 and administering it to the MS mouse models. Not only did the researchers discover that miR-219 led to the regeneration of myelin in the mouse models by reactivating oligodendrocyte function, it also improved the rodents’ limb function. These findings have now indicated a new direction towards a potential treatment for patients with MS.

Lu stated, “We show that miR-219 targets multiple processes that inhibit myelin formation after nerve injury by the disease process, and that treatment with this microRNA partially restores myelination and limb function. It is conceivable that augmenting miR-219 treatment with other blockers of myelin regrowth may provide a multipoint treatment strategy for people with demyelinating diseases like MS.”

However, the researchers cautioned that their study was conducted on mice models with MS, not with human models, so the findings cannot yet be applied to people. It is an exciting discovery in any case, and the team is now creating more compounds designed to stimulate miR-219 in humans to improve the possibility of treating the disease in human patients.

 

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