Researchers say they may have discovered a new therapeutic target for reducing the deterioriation rate of damaged brain cells and instead promoting their growth in multiple sclerosis (MS) patients.
The team that conducted the study, headed by Dr. Vittorio Gallo, director of the Center for Neuroscience Research at Children's National Health System, note that current therapies are effective for people with relapsing MS, but do little for promoting new tissue growth.
Our body fights this disease by trying to repair the damage MS causes. The brain creates new cells to replace the old ones; however, unknown factors halt this process and keep it from reaching its completion. MS causes random patches, or lesions, of brain inflammation, which leads to the destruction of myelin, the fatty insulation of nerve cell axons in the brain. Myelin is important in nerve cell function because it aids in the transmission of signals between neurons.
Gallo's research identified a protein with possible therapeutic potential that could promote repair of this damaged tissue, as publicized in the journal Neuron. That protein, Endothelin-1 (ET-1), inhibits myelin repair, but this study shows that blocking this ET-1 mechanism could have a reversal effect and actually promote myelin repair.
"We demonstrate," Gallo said in a statement, "that ET-1 drastically reduces the rate of remyelination." As such, ET-1 is "potentially a therapeutic target to promote lesion repair in deymyelinated tissue."
Endogenous oliogdendrocytle progenitor cells (OPCs) are involved in the repair of MS plaques in a process known as remyelination, in that they are supposed to differentiate. But in chronic MS, OPC differentiation is arrested, and that's why current MS therapies, Gallo says, "have little impact in promoting remyelination in tissue."
The goal of this study was to target ET-1 by identifying cell signals that could promote lesion repair. Gallo believes it could play a "crucial role in preventing normal myelination in MS and in other demyelinating diseases."
