Glucosamine, the over-the counter natural product that has been touted to help with joint and cartilage problems associated with arthritis, may also provide some relief to individuals with multiple sclerosis (MS), a degenerative, nervous system disease with no known cure.

Using a mouse model of MS, neurologists at Jefferson Medical College found that doses of glucosamine similar to those taken for osteoarthritis dramatically delayed the onset of symptoms and improved the animals’ ability to move and walk.

The scientists, led by A. M. Rostami, M.D., Ph.D., professor and chair of the Department of Neurology at Jefferson Medical College of Thomas Jefferson University and the Jefferson Hospital for Neuroscience in Philadelphia, and Guang-Xian Zhang, M.D., Ph.D., assistant professor of neurology at Jefferson Medical College, say the treatment’s anti-inflammatory effects may be useful in conjunction with more mainstream therapies such as beta-interferon in helping patients with MS to delay or perhaps stave off some of the debilitating effects of the disease. They report their findings in the December 1, 2005 of The Journal of Immunology.

“It would be fantastic if glucosamine works in humans because we have a product that has a long track record for safety, and most importantly, can be given orally,” says Dr. Rostami, who is also director of the Neuroimmunology Laboratory in the Department of Neurology at Jefferson Medical College. He notes that current treatments for MS are given by injection. He hopes to test glucosamine in clinical trials in the near future.

MS, one of the most common neurological diseases affecting young adults, is thought to be an autoimmune disease (in which the body attacks its own tissue) affecting the central nervous system (CNS). In MS, the myelin coating of nerve fibers becomes inflamed and scarred. As a result, “messages” cannot be sent through the nervous system.

Dr. Rostami and his group used an animal model of MS called experimental autoimmune encephalomyelitis (EAE), which mimics the human disease, to investigate glucosamine’s potential immune system-suppressing properties. Such animals gradually develop the disease.

In the studies, some of the mice received glucosamine, while others did not.

They gave glucosamine to the mice three ways: orally, intraperitoneally and intravenously. They also tested the drug in one set of animals before the onset of symptoms, and in another group at the time the animals began to show symptoms.

In each case, the researchers showed they could significantly prolong the onset of disease. That is, those animals that got glucosamine took longer to get ill and once they became ill, the disease was much less severe. It was just as effective when given early in the disease or when the animals became sick.

They examined the animals’ spinal cords and found less inflammation and “demyelination” in those that were given glucosamine.

“As a therapy, it might be used in combination with other proven treatments, such as beta-interferon and copaxone,” says Dr. Rostami.

The research team has some ideas of how glucosamine exerts its effects. According to Dr. Rostami, EAE and MS are caused by abnormal responses from the immune system’s T cells. There are two types: TH1, which promotes inflammation, and TH2, which is anti-inflammatory. “We’ve shown the glucosamine modulates the immune response by producing more TH2 responses, suppressing brain inflammation,” he says. “At the same time, it suppresses TH1 response.”

The researchers currently are testing the effectiveness of combinations of glucosamine and standard drugs for MS in the same mouse model to look for adverse effects. They are also trying to find out if glucosamine can suppress the relapses in the relapsing/remitting form of the disease.

Relapsing/remitting is the most common form of MS. Patients experience clearly defined “flare-ups,” acute episodes in which neurological functions worsen, followed by partial or complete recovery periods.