MS protein offers hope for new generation of drugs

By
Sunday, 14 September, 2003

Monash University researchers, using synchrotron radiation, have unravelled the structure of a protein that plays a crucial role in multiple sclerosis (MS), a finding that could eventually lead to the development of better drugs for treating this disease.

MS is an inflammatory autoimmune disease of the central nervous system (brain and spinal cord) that is characterised by the destruction of the protective sheaths that surround nerve cells. The progress, severity and specific symptoms of the disease cannot be predicted and symptoms can range from tingling and numbness to paralysis and blindness.

A team of Monash research fellows - Dr Hugh Reid, Dr Craig Clements and Dr Travis Beddoe - headed by Dr Jamie Rossjohn from the Protein Crystallography Unit in the Department of Biochemistry and Molecular Biology and Professor Claude Bernard from La Trobe University, collaborated to solve the structure of a protein called MOG (myelin oligodendrocyte glycoprotein) which is found on the outer most part of the myelin sheath that protects nerve cells.

"The cause of MS is unknown but what is known is that in people with MS, the body recognises MOG as foreign and the protein is attacked by the immune system," said Dr Rossjohn.

"The function of MOG is also unknown. It could be involved in maintaining the myelin sheath that protects nerve cells or it could be involved in the signalling process that tells myelination to cease. Now we have solved the structure of MOG we will be able to gain greater insight into its normal function and its role in pathology."

Dr Rossjohn is hopeful the university's studies of MOG could lead to better treatments for MS. "The main treatment for MS is interferon but these drugs work only in about 40% of patients. Although they lengthen the time between attacks they don't prevent them from occurring and don't prevent progression of the disease to the more chronic form," he said.

"Now we know the precise shape of MOG we might be able to design therapeutics that interfere with T cell attack (T cells are a part of the immune system response) or prevent the destructive action of the antibodies that bind to MOG, thereby halting the progress of MS."

Item provided courtesy of Monash University

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