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Protein May Repair Brain Tissue Damaged by Multiple Sclerosis, Study Says

First Posted: Feb 07, 2014 04:59 PM EST
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Multiple Sclerosis is an autoimmune disease that affects the brain and spinal cord, destroying tissue and cells along the way. Previous research and practices have found that therapies can help with relapses of MS, but cannot help repair the tissue and cells that have been affected.

Vittorio Gallo, PhD, is the Director of the Center for Neuroscience Research at Children's National Health System. He and his researchers believe to have found what they call a "potentially novel therapeutic target." This would not only lessen the rate of deterioration of brain cells caused by MS, but it would help new growing cells complete the repair of the previously damaged ones.

After MS has affected the body and caused cell damage, the brain produces new cells to repair the old ones. However, a majority of cases has shown that there are unknown factors that hinder the cells from completely repairing, thus creating a permanent loss. The brain inflammation caused by MS leads to the destruction of myelin, which is the fatty insulation for the axon nerve fibers in the brain, thus destroying brain cells. A molecule known as Endothelin-1 (ET-1) is known to inhibit the repair of the myelin.

Yesterday, Gallo and his team of researchers reported their findings in Neuron and cited the effectiveness of a certain protein that could help fully repair previously damaged cells. This protein, known as "ET-R antagonist PD142,893" can be used therapeutically to promote remyelination and effectively block ET-1 from inhibiting cell repair.

"We demonstrate that ET-1 drastically reduces the rate of remyelination," Gallo said. "ET-1 is potentially a therapeutic target to promote lesion repair in deymyelinated tissue.  It could play a crucial role in preventing normal myelination in MS and in other demyelinating diseases," Gallo said in this Children's National Health System article.

To read more about Dr. Gallos study, visit the link above as well as yesterday's published study in Neuron.

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