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Friday, February 14, 2014

Targeting Et-1 May Reverse Myelin Deterioration in Multiple Sclerosis

Posted by: Maureen Newman February 11, 2014
Myelin and multiple sclerosisScientists at the Center for Neuroscience Research at Children’s National Health System know it is better to treat a disease than to only treat the symptoms. Vittorio Gallo, director of the center, just published research in the journal Neuron that could lead to pharmaceuticals that reduce the rate of deterioration and actually promote growth of neurons damaged by the disease multiple sclerosis (MS).
MS is an autoimmune disease where the myelin sheath around axons is destroyed, and unable to be repaired by the body. This is because endogenous oligodendrocyte progenitor cells (OPCs), cells that give rise to other cells (oligodendrocytes) that myelinate axons in the central nervous system, fail to differentiate into effective myelinating cells. This results in chronic lesions in the brain, or deterioration that affects everything from afflicted patients’ speech to their motor coordination.
Dr. Gallo, who also serves as a professor of pediatrics at the George Washington University School of Medicine and Health Sciences (SMHS), reported in the research publication that he and his fellow researchers were able to identify a small protein that can be targeted to promote repair of damaged tissue, with therapeutic potential. The molecule, Endothelin-1 (ET-1), is shown to inhibit repair of myelin.
BioNews Texas has recently covered several promising research stories on how focusing on myelin repair and neural protection is quickly becoming the vanguard of Multiple Sclerosis research and development, as myelin damage is a hallmark characteristic of MS. The study demonstrates that blocking ET-1 pharmacologically or using a genetic approach could promote myelin repair.
“We demonstrate that ET-1 drastically reduces the rate of remyelination,” Gallo said. This creates a new drug target in the treatment of MS. Said Gallo, ET-1 is “potentially a therapeutic target to promote lesion repair in deymyelinated tissue.” It plays a “crucial role in preventing normal myelination in MS and in other demyelinating diseases.”

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