Multiple Sclerosis Nerve Damage Repaired By Scientists

Nerve damage which was caused by multiple sclerosis (MS) was repaired by scientists from the Mayo Clinic, Rochester, USA, who were working with mice. The scientists said it is hoped this may lead the way to new treatments for humans.

The immune system of a MS patient attacks the fatty myelin sheath which covers the nerves, gradually destroying them. The patient's nerves do no work properly; he/she experiences loss of balance, blurred vision, and sometimes paralysis. The symptoms can be treated/managed to some extent; however, there is no modern way to repair damaged myelin.

In this latest experiment, the scientists re-grew myelin in mice with MS by using a human antibody. At the American Neurological Association meeting they explained that they would be starting human trials after further tests are carried out on animals.

The scientists said that although this technique of using natural human antibodies to treat MS has never been tested in humans, they believe their findings are very promising.

The human body generally is able to repair myelin as and when required - unfortunately, this is not the case with the MS patient; for them the myelin repair process occurs very slowly or fails altogether. In this experiment, the researchers used an antibody that was genetically engineered from a single cell and managed to get the repair underway in mice with MS. The antibody continued working even while the mice were undergoing steroid treatment with methylprednisolone. Humans with MS frequently have to take steroid treatment.

"The repair of chronic spinal cord injury is seldom modeled in laboratory studies, but it is an important reality for the treatment of humans. The concept of using natural human antibodies to treat disease of this kind has not yet been tested in humans, but these research findings are very promising," said author, Moses Rodriguez, M.D., a Mayo Clinic neurologist.

The study used laboratory mouse models of chronic progressive multiple sclerosis in humans. The scientists defined the severity of the disease and treatment success by measuring how naturally active the mice were, especially at night as mice are nocturnal animals.

Each mouse received a single dose of the antibody. The researchers explained that a minimum of 25 mcg/kg was required to trigger remyelination (myelin repair) - this would be the equivalent to approximately 2 mg for an average adult (a very low dose). The myelin repair plateaued after five weeks in the mice models.

The researchers explained that as the protein is a naturally occurring one of the immune system, it does not seem to bring with it any side effects. However, it would have to be tested on humans.

In short, this antibody:

-- Triggers remyelination with a single 25 mcg/kg dose in mice models
-- The remyelination tapers off at five weeks after a single dose
-- Converts a model of chronic immune mediated demyelination to one that repairs with the speed of a toxin induced model of demyelination

This study was funded by the NIH (National Institutes of Health), the National Multiple Sclerosis Society, Multiple Sclerosis Society of Canada, the Hilton Foundation, and Mr. and Mrs. Eugene Applebaum.

-- http://www.mayoclinic.org
-- American Neurological Association - 132nd Annual Meeting