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About Sickkids
About SickKids

February 26, 2009

New insight into MS – Researchers shed light on an underlying cause of damage to the nerve coating

A team of scientists has found changes in the amount, or charge, of a protein may cause the breakdown of myelin – the protective casing that surrounds nerve fibres – in MS patients. The study is published in the advance online edition of Proceedings of the National Academy of Sciences of the United States of America.

Researchers from the University of California at Santa Barbara and The Hospital for Sick Children (SickKids) examined the impact of changing the levels of myelin basic protein (MBP) – a protein that is abundant in the brain and is the second most abundant protein in myelin.

In the central nervous system, MBP plays a key role in holding together the myelin sheath – a multi-layered, protective casing that surrounds nerve axons (nerve fibres). In MS, the myelin sheath is destroyed, resulting in impaired nerve conduction and nerve degeneration.

Using sophisticated biophysical measurements, researchers altered the amount of MBP, then measured the positive and negative forces between synthetic myelin membranes. They found that if the balance is altered, the membranes separate and swelling occurs. A disturbance of this balance could occur in MS cases.

“Modifying the amount, or charge, of MBP could lead to the swelling, vacuolization (the formation of fluid-filled pockets within myelin), and eventual disintegration of myelin, which is what occurs in MS,” says Dr. Joan M. Boggs, SickKids Senior Scientist and Professor of Laboratory Medicine and Pathobiology at the University of Toronto.

“The study also suggests a potential therapeutic approach for the disease. Myelin swelling could possibly be counteracted by using drugs called osmolytes.”

Such an approach, which involves extracting the excess fluid from diseased myelin, has been successfully used to treat spinal cord injuries in animals, says Dr. Boggs. In the case of MS, a method to enable the drug to reach the human brain would have to be developed. Furthermore, it would be necessary to treat patients at an early stage of the disease before the breakdown of myelin and nerve axons had occurred.

The research was supported by the National Institutes of Health, Canadian Institutes of Health Research, and SickKids Foundation.

For more information, please contact:

Suzanne Gold
The Hospital for Sick Children
Phone: 416-813-7654 ext. 2059
email: suzanne.gold@sickkids.ca