Submitted to Coalition website by Denise Nichols, Chair Gulf War Illness
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CHICAGO (AFP) A new drug currently being tested in humans has been found to suppress multiple sclerosis and other auto immune diseases in mice, according to a study published Monday.

The drug works by stimulating the development of t-cells, a kind of white blood cell which helps the immune system target specific pathogens.

"We know that it generates t-cell lines that are regulatory for auto immune diseases and that the same t-cell line will suppress three different auto immune diseases in mice," said study author Jack Strominger of Harvard University.

"It is also effective in several other auto immune diseases in mice, so it's possible this class of molecules could be more broadly used than simply for multiple sclerosis."

Strominger and his team developed a relative of the drug Copaxone which is currently used to treat multiple sclerosis.

They tested it on mice directly and then generated a t-cell line from those treated mice. Those t-cells suppressed the disease in three different models, he said in a telephone interview.

In testing it on mice they discovered it was "far more effective" in treating multiple sclerosis and "amazingly more effective" in treating uveitis, a common cause of blindness, he said.

"Whether this relative or another one is going to replace Copaxone, I don't know but there are certain to be second or third generation drugs in this category," he said.

"Mice are not man and the only way to find out whether FYAK is more effective than Copaxone is to do a clinical trial."

A small company near Harvard is currently testing the drug in humans in a Phase I clinical trial, he said.

It could take years to prove if the drug is both safe and effective.

The study was published in the early edition of the Proceedings of the National Academy of Sciences.

Potential New Target For Multiple Sclerosis Therapy
ScienceDaily (Mar. 30, 2008) Researchers demonstrate both genetic and pharmaceutical evidence for the role of a protein called collagenase-2 in the development of multiple sclerosis (MS), providing a potential new way to combat this debilitating disease.

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See also:
Health & Medicine
Multiple Sclerosis Research
Nervous System
Diseases and Conditions
Mind & Brain
Huntington's Disease
Multiple Sclerosis
Disorders and Syndromes
Reference
Huntington's disease
Biological tissue
Stem cell treatments
Tissue engineering
Collagenase-2 is a member of a protein family called matrix metalloproteinases (MMPs, collagenase-2 is MMP8), a large group of enzymes that break down collagen and other components of the body's connective tissue. MMPs have been implicated in contributing to MS by degrading the tissue that maintains the blood-brain barrier, thus allowing unwanted cells to invade and break down nerves. In fact, MMPs are found in elevated amounts in the blood and spinal fluid of diseased individuals.

Using a mouse model of MS, Carlos Lopez-Otin and colleagues performed two analyses on MMP8 to determine how relevant this protein is to the disease. First, they developed mutant mice deficient in the gene for MMP8 and found that these mice had a fewer invading cells in the brain, fewer damaged nerves, and a general improvement in their clinical profile.

They also gave diseased mice a drug that blocked MMP8 activity and found that this, too, could reduce the severity of disease symptoms. Taken together, these promising findings provide the first causal evidence for MMP8 in the development of MS, and offer a new therapeutic target.

Adapted from materials provided by American Society for Biochemistry and Molecular Biology, via EurekAlert!, a service of AAAS.

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