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SLU researchers show how to stop muscle weakness caused by myasthenia gravis
Date:12/20/2007

Severe muscle weakness caused by myasthenia gravis a highly debilitating autoimmune disorder can be prevented or reversed by blocking a key step in the immune response that brings on the disease, researchers at the Saint Louis University School of Medicine have found.

Myasthenia gravis, which affects about 120,000 Americans, is caused when the immune system produces antibodies that attack and damage acetylcholine receptors, which are mechanisms that play a key role in transmitting the electrical impulses that cause muscles to move and contract.

The immune response at the heart of this process is called a complement cascade a complex chain of chemical reactions in which proteins bind together to attack a cell by punching a hole in it. When acetylcholine receptors are damaged in this way, muscle movement is severely impaired.

Using an animal model, the SLU scientists found they could prevent muscle weakness, or restore muscle strength, caused by myasthenia gravis by stopping the complement cascade at a step called C5 before the series of chemical reactions had finished. They did this by administering an anti-C5 agent, which targets one of the proteins involved in the cascade and thus stops the process.

The researchers findings are published in a recent edition of the Journal of Immunology (http://www.jimmunol.org/cgi/reprint/179/12/8562).

Henry J. Kaminski, M.D., professor and chairman of the department of neurology and psychiatry at the Saint Louis University School of Medicine, one of the studys authors, said the findings are promising enough that human clinical trials involving the anti-C5 agent called eculizumab are likely within a year.

We believe this therapeutic approach has strong potential for improving the lives of patients with myasthenia gravis, Kaminski said. And if it proves successful there, it could also one day hel
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Contact: Donn Walker
dwalke18@slu.edu
314-977-8015
Saint Louis University
Source:Eurekalert

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