Apr
25
If finding a way to restore nerve cells’ protective coating were the only challenge, multiple sclerosis would be a more manageable disease.
But researchers at the UConn Health Center say MS also takes it toll on axons, the nerve cell extensions that carry nerve impulses.
The devastation hinders the ability of neurons to communicate with each other, resulting in debilitating neurodegenerative disease.
“The long-term disability of MS is caused by degeneration of axons that have lost their myelin sheath – their protective coating,” says Rashmi Bansal, an associate professor of neuroscience.
Bansal recently won a grant from the National Multiple Sclerosis Society for her research focusing on a specific protein and its role in MS.
In MS patients and mouse models, this protein, called fibroblast growth factor, increases in areas of the nervous system where the myelin is missing.
“There’s got to be an important connection of this observation with the disease scenario,” Bansal says.
Signals from these growth factors regulate the biology of cells called oligodendrocytes, which produce myelin in the central nervous system.
Fibroblast growth factors bind and signal to oligodendrocytes through three different receptors, which are the docking sites for these growth factors. Bansal’s previous research found this interaction varied depending on the receptor involved.
“Stimulation of one receptor versus the other led to different responses,” Bansal says. “And interestingly, we found that in oligodendrocytes, while one response was positive, the other was a negative pathological one.
So that raises the question of what the fibroblast growth factor is doing. Is it good or bad to have a lot of it in MS lesions?”
read more: UConn Advance – April 28, 2008 – Neuroscience researcher working toward a cure for MS
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