News Release

Mayo Clinic scientists discover way to enhance immune system that repairs nervous system in mouse model

Peer-Reviewed Publication

Mayo Clinic

ROCHESTER, MINN. -- In a major scientific discovery, Mayo Clinic scientists conducting research in mice with central nervous system damage have found a way to enhance the immune system that resulted in nervous system repair in the mice. The study detailing the findings will be published in the Tuesday, June 6 edition of Proceedings of the National Academy of Sciences.

In their study, Mayo Clinic scientists identified two natural human antibodies that, when given to mice with a chronic, demyelinating disease, caused the regrowth and repair of the myelin sheath. Myelin surrounds nerve fibers and acts as "insulation," allowing them to function properly. Previously, it was thought that damage to myelin was permanent and repair to the nervous system was not possible. In humans, damage to the myelin sheath can be caused by traumatic injury or by diseases such as multiple sclerosis, transverse myelitis and other demyelinating or genetic conditions.

"Clearly, our study shows that the two natural human antibodies, when introduced into mice that had nervous system damage, safely caused substantial repair to the myelin and the nervous system," says Moses Rodriguez, M.D., a Mayo Clinic neurologist and the principal author of the study. "This is a significant step forward in our understanding of the nervous system and the immune system. Whereas we know that the immune system can have a protective effect on the body, we now are beginning to discover that the immune system may be harnessed to effect repair to the nervous system in the mouse model."

In the laboratory study, mice were injected with a virus that caused demyelination in the nervous system similar to the damage multiple sclerosis causes in humans. The mice were treated with two natural human monoclonal antibodies after the onset of demyelination. This treatment promoted remyelination to an equivalent or greater extent than human intravenous immunoglobulin (IVIg), an established treatment for immune-mediated diseases. The antibodies bound to the surface of the cells that make myelin.

The research also yielded the molecular sequence of the antibody which will facilitate production of the antibody in large quantities for further studies. Treatment with the human antibodies proved to be safe in mice.

Currently, there is no new treatment or therapy for humans as a result of this research. It is unknown how long the development of the clinical trials will take or when the clinical trials would begin.

Funding for the first stage of research was provided by the National Institutes of Health, National Multiple Sclerosis Society, Mayo Foundation and Acorda Therapeutics. Acorda Therapeutics is a biotechnology company that develops therapeutic products for spinal cord injury and other central nervous system conditions. Acorda is planning to complete the preclinical work necessary before human clinical trials can be designed. This work includes scaling up manufacturing of the antibody to produce quantities sufficient for human clinical trials, and conducting formal toxicity and pharmacokinetic studies.

Ron Cohen, M.D., Acorda's president and CEO, states, "Acorda is proud of its collaboration with Dr. Rodriguez and Mayo Clinic. The identification of this human monoclonal antibody is a significant step forward in its development as a potential therapy for people with demyelinating conditions, such as multiple sclerosis."

"This type of basic scientific research is needed to advance medicine and our potential to develop new treatments and therapies for humans," says Dr. Rodriguez.

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Contact:
Jane Jacobs
507-284-2387 (days)
507-284-2511 (evenings)
e-mail: newsbureau@mayo.edu

John Murphy
507-538-1385 (days)
507-284-2511 (evenings)
e-mail: newsbureau@mayo.edu

NOTES:
For more information, audiences may be referred to Mayo Clinic website (http://www.mayo.edu) or Acorda Therapeutics (http://www.acorda.com)

For advance, embargoed copies of the research paper, please contact: David Schneider Proceedings of the National Academy of Sciences 202-334-2138 (phone)


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