Multiple sclerosis (MS) is one of a number of diseases related to accelerated loss of the myelin sheathing of nerves. This loss occurs in everyone to a much lesser degree during aging - there are many medical conditions that, once you look into the mechanisms, turn out be the consequences of an acceleration of a universal process. So we should keep an eye on work aimed at the regeneration of myelin, as it may have broader applications than treating MS:
Researchers have found a "potentially novel therapeutic target" to reduce the rate of deterioration and to promote growth of brain cells damaged by multiple sclerosis (MS). 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. 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.
Repair of damaged MS plaques is carried out by endogenous oliogdendrocyte progenitor cells (OPCs) in a process called remyelination. Current MS therapy can be effective in patients with relapsing and remitting MS, but "have little impact in promoting remyelination in tissue." Several studies have shown that OPCs fail to differentiate in chronic MS lesions.
Targeting ET-1 is a process that involves identifying signals in cells that could promote lesion repair. "We demonstrate that ET-1 drastically reduces the rate of remyelination. [It] is potentially a therapeutic target to promote lesion repair in deymyelinated tissue [and] could play a crucial role in preventing normal myelination in MS and in other demyelinating diseases."