December - 2008

Young Researchers Shine

The MS - Society's 2008 National Conference brought together nearly a hundred young research fellows to add their voices and talents to solving the puzzle of MS. History shows that scientific breakthroughs often come from new thinking, fresh ideas, and young people. The conference is encouraging young scientists ready to embark on careers in biomedical research to focus on the final path of finding the way to stop MS in it's tracks.

The conference aimed to promote the sharing of research information among research fellows and faculty grant recipients, develop a sense of community among investigators, stimulate new research ideas, and strengthen commitment to MS research.

"I'm new to the field of MS, and I'm gratified to see how collaborative everyone is," said Daniel C. Tanner, PhD, a fellow at the University of Rochester.

Twenty-one fellows presented their work on strategies to stop immune attacks against myelin and other central nervous system tissues in MS, including:

>< Yueting Zhang, PhD (Mount Sinai School of Medicine) presented findings from a team led by her mentor Gareth John, VetMB, PhD, on immune messenger protein interleukin-11. The team found that this protein promotes the survival and maturation of myelin-making cells, leading to increases in myelin formation in tissue samples from people with MS.

>< Philip L. Jager, MD, PhD (Brignam & Women's Hospital) reported on his team's finding that CD58, a possible location for one of many MS susceptibility genes, appears to contain genetic variations relevant to inflammation as well as nerve degeneration, but that these may be genetically distinct processes.

>< Ellen Mowry, MD (University of California, San Francisco), a Sylvia Lawry Physician Fellow training to conduct MS clinical trials, presented her team's findings that someone whose initial MS event is resolving the unpredictability of MS.

"You can read about MS in medical papers," said fellow Jennifer Kanter, PhD, of Harvard University. "But what you learn from talking to someone with the disease is so much more real." Dr. Kanter, whose father had MS, encouraged her colleagues to participate in Walk MS and Bike MS. She participates in the 50-mile Challenge Walk with her mother and sister. "If you want to feel the happiness that you get when an experiment goes well, go to a National MS Society event -- you'll feel it every time!" she said.

A second Fellows Conference is planned for 2010, "It was great to meet so many people who have a common passion," said Astrid Cardona, PhD a Career Transition Fellow at the Cleveland Clinic Foundation. "How could we fail with all those great people behind us!"

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November - 2008

Leukemia drug can halt, reverse MS

LONDON (AFP) - Researchers at the University of Cambridge said Thursday they have found that a drug originally developed to treat leukemia can halt and even reverse the debilitating effects of Multiple Sclerosis (MS).

In trials, alemtuzumab reduced the number of attacks in sufferers and also helped them recover lost functions, apparently allowing damaged brain tissue to repair so that individuals were less disabled than at the start of the study. "The ability of an MS drug to promote brain repair is unprecedented," said Dr. Alasdair Coles, a lecturer at Cambridge University's department of clinical neuroscience's, who coordinated many aspects of the study. "We are witnessing a drug which, if given early enough, might effectively stop the advancement of the disease and also restore lost function by promoting repair of the damaged brain tissue."

The MS Society, Britain's largest support charity for those affected by the condition, said it was "delighted" at the trial's results, which must be followed up with more research before the drug can be licensed. "This is the first drug that has shown the potential to halt and even reverse the debilitating effects of MS and this news will rightly bring hope to people living with the condition day in and day out," said head of research Lee Dunster.

MS is an auto-immune disease that affects millions of people worldwide, including almost 100,000 in Britain and 400,000 in the United States. It is caused by the body's immune system attacking nerve fibres in the central nervous system, and can lead to loss of sight and mobility, depression, fatigue and cognitive problems. There is NO cure, and few effective treatments.

In the trial, 334 patients diagnosed with early-stage relapsing-remitting MS who had not previously been treated were given alemtuzumab or interferon beta-1a, one of the most effective licensed therapies for similar MS cases. After three years, alemtuzumab was found to reduce the number of attacks the patients suffered by 74% over the other treatment, and reduce the risk of sustained accumulation of disability by 71% over interferon beta-1a. Many individuals who took alemtuzumab also recovered some of their lost functions, becoming less disabled by the end, while the disabilities of the other patients worsened, the study in the New England Journal of Medicine said.

Alastair Compston, professor of neurology and head of the clinical neuroscience's department at Cambridge, said alemtuzumab was the "most promising" experimental drug for the treatment of MS. He expressed hope that further trials "will confirm that it can both stabilize and allow some recovery of what had previously been assumed to be irreversible disabilities."

Alemtuzumab was developed in Cambridge and has been licensed for the treatment of chronic lymphocytic leukemia.