New researchers will join team to tackle crippling disease



A group of Yale researchers was recently awarded an $875,000 grant that will provide for a large-scale, multidisciplinary study of prevention and treatment of Multiple Sclerosis.

The grant, called the Collaborative Multiple Sclerosis Research Center Award, given by the National Multiple Sclerosis Society, will allow three Yale scientists who are not currently working on Multiple Sclerosis, or MS, research to join labs already examining the disease. Beginning April 1, the projects will continue for five years.

“It’s collaborative and synergistic — there are already fantastic scientists here, we just have to bring them together,” said Dr. Nancy Ruddle, professor of epidemiology and public health and immunobiology. “There are many smalls parts of this that have to do with providing core research facilities to everybody, and — to raise the visibility for the research.”

MS is an autoimmune disease in which the body attacks the myelin sheath — a fatty tissue that covers the nerve fibers of the central nervous system (CNS) and helps cells conduct electrical impulses. This attack disrupts the ability of the nerves to conduct electrical impulses, resulting in problems with cognitive function, muscle control, and vision. The disorder effects an estimated 2.5 million people worldwide, according to the National Multiple Sclerosis Society’s Web site.

“It’s a disease that really touches many of us here,” said Jeffery Kocsis, professor of neurology and neurobiology at Yale. “The disease will manifest itself [when patients are in their] 20s and 30s — what’s devastating, from a social perspective, is that someone is just getting their family started, and booming in their career, and then they present with signs of MS — It has a large effect on our society, socially, psychologically and economically.”

The three Yale researchers not currently involved in MS studies, who will join the collaborative research program, are Diane Krause, associate professor of laboratory medicine and pathology, Peter Creswell, professor of immunobiology, and Richard Flavell, chair of immunobiology. Albert Lo, assistant clinical professor of neurology, will also work on the project. They will join projects in existing MS research groups headed by Ruddle, Kocsis and chairman of neurology Dr. Stephen Waxman.

Creswell is an expert in antigen presentation, and will contribute to the study of CNS damage, and how antigens are presented in the brain. Flavell is an expert in animal models, and will aid in testing hypotheses related to clinical disease. Krause specializes in stem cells, which may be useful in the repair of CNS damage, and myelin loss.

The various projects will concentrate on prevention of disease progression and on myelin repair.

“We can not only prevent disease — and find potential ways to block immunological assault on myelin,” Kocsis said. “Part of the approach we have taken in the labs is to find ways to repair the damaged region [of patients' myelin], to restore some function — or find pharmacological approaches to improve impulse progression — We are trying to bridge two important areas — the immunological approach and the biophysical, pharmacological, structural approach.”

Researchers said they hope to develop better MS treatments, and ultimately, a cure. Previous studies, specifically ones conducted by Waxman, have shown encouraging potential for recovery in MS patients.

“What’s interesting is that in very few neurological diseases do we see recovery after the nerve cells have been damaged, but we do see it in MS — it’s called remission,” Waxman said. “Me and my colleagues worked out how remissions occur — and now, we want to induce remissions.”

The researchers’ finding may help the development of better MS treatments, which may also have applications in other autoimmune diseases like rheumatoid arthritis and lupus.

“They’re all going to be a little different, because in MS the antigen being attacked is in the nervous system, but in arthritis, and even diabetes, the antigen will be other cells in the body — but fundamental mechanisms will have some commonality,” Kocsis said. “A breakthrough in one disease might be helpful in developing approaches for another disease.”

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