Wednesday, November 19, 2003
A drug used to treat multiple sclerosis has been found to stimulate immune system cells to produce a brain-protecting protein.
Researchers at the University of Maryland School of Medicine have shown that the drug, Copaxone, stimulates T cells to produce a protein called brain-derived neurotrophic factor.
"Our findings seem to suggest a possible neuroprotective mechanism for Copaxone based on its ability to stimulate production of BDNF, a potent neurotrophin that has profound effects on neuronal survival and repair," says researcher Suhayl Dhib-Jalbut.
Nervous system damage
Multiple sclerosis is a chronic disease of the central nervous system characterized by damaged myelin—a protective sheath surrounding nerve fibers in the central nervous system. Faulty myelin leads to interference with messages between the brain and other parts of the body.
Common symptoms of the disease include fatigue, weakness, spasticity, balance difficulties and depression.
Copaxone is the brand name for a synthetic chemical called glatiramer acetate that's used to modify the course of multiple sclerosis. While its exact mechanism of action is unknown, the drug has been shown to reduce the relapse rate in people with the relapsing-remitting form of the disease.
"It is important to further understand mechanisms that produce clinical effects of drugs used to treat MS," says Dhib-Jalbut. "Our findings seem to suggest a possible neuroprotective mechanism for Copaxone based on its ability to stimulate production of BDNF, a potent neurotrophin that has profound effects on neuronal survival and repair."
Brain-derived neurotrophic factor is a molecule thought to be of particular importance in multiple sclerosis because of the role it plays in the growth, development, maintenance and function of neurons.
In addition, it is hypothesized that locally produced brain-derived neurotrophic factor might affect the rebuilding of myelin.
In their study, Dhib-Jalbut and colleagues examined the protein's production in the T cells of 12 multiple sclerosis sufferers.
They found that Copaxone spurred some T cells to produce significantly more brain-derived neurotrophic factor, suggesting that the drug has a possible neuroprotective action.
While the drug's exact mechanism of action isn't fully understood, it
"may work through a dual action of anti-inflammatory and neuroprotective
mechanism via activation of T cells which enter the brain and protect axons
from long-term degeneration," says Dhib-Jalbut.
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