A new study suggests that a viral protein that exists in human genetic material may play a key role in the development of multiple sclerosis (MS).1
A Protein Link to MS Postulated
Doctors at the University of Calgary in Alberta, Canada found that the protein called syncytin (SIN-seh-tin) may be linked with the damage that occurs in myelin in a person's central nervous system when MS occurs.
Multiple sclerosis involves a direct attack, thought to be initiated by the immune system, on myelin, a fatty substance that acts as a protective sheath around nerve cells. Myelin not only plays this protective role, it also helps nerves conduct electrical impulses between one another. When myelin is attacked and stripped away in MS, it leaves these nerve cells exposed and unable to communicate with each other. The result is the signs and symptoms seen in MS.2
Syncytin's Link to Oxidation
In learning the role of syncytin in this disease, the Calgary medical researchers examined brain tissue from a small number of people with MS, comparing it to that of people with other neurological diseases or no disease at all. They found that there were significantly higher levels of this protein in the tissue taken from people with MS. That also found that syncytin was located near areas where myelin damage had occurred.
It was also learned that syncytin induced oxidation, the process of physiological damage that occurs by harmful molecules called free radicals. The researchers found that adding synctyin to samples of myelin-making cells resulted in the death of these cells. In mice with a disease similar to MS, the researchers found that injecting a syncytin-producing virus resulted in myelin damage and impaired motor function.
However, when an antioxidant known as ferulic acid was given to the rodents and introduced to the myelin-producing cells, the treatment significantly reduced the death of the cells, and the motor abnormalities in the mice improved.
"Syncytin's proinflammatory properties in the nervous system demonstrate a novel role for an endogenous retrovirus protein, which may be a target for therapeutic intervention," the medical scientists wrote.
Critics: Still Unanswered Questions
In an editorial about the study published in the same journal,(3) Mark Mattson, PhD, and Dennis Taub, PhD, both of the National Institute on Aging at the National Institutes of Health noted that although this study did find an association between syncytin and the inflammatory processes that occur in the early development of multiple sclerosis, it did not establish a role for this protein in the development of the disease. In order to do that, further studies are needed, they said.
For example, determining whether blocking syncytin improves mouse models of MS (a disease similar in pathology to MS called experimental autoimmune encephalitis (EAE) is typically introduced to mice in scientific studies of MS), and whether cells that make up the immune system in people react to the presence of this protein are necessary research steps that must be undertaken before any firm conclusions can be drawn, Mattson and Taub stressed.
Nevertheless, they say, if the interesting findings of this study can be confirmed and expanded on, it may open new avenues of investigation into the underlying pathology of MS, and may suggest targets for new treatment approaches.
1. Antony JM, Van Marle G, Opii W et al. Human endogenous retrovirus glycoprotein-mediated induction of redox reactants causes oligodendrocyte death and demyelination. Nat Neurosci 2004 Oct;7(10):1088-95.
2. National Multiple Sclerosis Society. What is Multiple Sclerosis?
John Martin is a long-time health journalist and an editor for Priority Healthcare. His credits include coverage of health news for the website of Fox Television's The Health Network, and articles for the New York Post and other consumer and trade publications.
