UMDNJ researchers have identified a key pathway that could lead to new therapies to repair nerve cells' protective coating stripped away as a result of autoimmune diseases such as Multiple Sclerosis (MS). An article reporting their findings will appear in the May 13 online edition of the Journal of Neuroscience.
Myelin is fatty material that coats and protects the ends of nerve cells. The loss of myelin and myelin-producing cells impairs the ability of nerves to conduct signals. A severe loss may lead to erosion of nerve tissues and result in permanent damage.
"In people with MS that is relapsing-remitting, the body can replace myelin that has been stripped away," explained Teresa L. Wood, Ph.D., the study's lead investigator. "But, after repeated attacks, that process of replacement no longer functions well," she added.
"Our data demonstrate that a novel cellular pathway, called the mammalian target of rapamycin (mTOR), regulates the generation of new myelin-producing cells (oligodendrocytes) and the production of myelin in immature rodent cells," Wood said. She is a professor in the Department of Neurology & Neurosciences and the Rena Warshow Chair in Multiple Sclerosis at the UMDNJ-New Jersey Medical School.
More work is needed to determine if the key to reactivate remyelination is to stimulate the pathway or if environmental impediments, such as inflammation, also must be overcome to allow the pathway to function normally. "Now at least we know a target to go after to promote repair," she said.
The researchers' work may also lead to new therapies for other disorders where the myelin-producing cells are affected, such as autism, Alzheimer's disease, and perinatal brain injury.