Disabling brain conditions like multiple sclerosis are generally caused by the activation of the immune system in some genetically susceptible individuals. However, research scientists are certain that some environmental factors can also play a significant role in the pathogenesis of multiple sclerosis. The disorder is marked by degenerative damage to protective myelin sheaths that protect nerves entering and exiting the brain or spinal cord.
The higher degree of morbidity and chronic progressive course of the disease has prompted scientists to conduct extensive research to identify potential drug targets for treatment of Multiple Sclerosis. The latest research conducted by investigators at Children’s National Health System may potentially improve outcomes for patients of MS.
Research Background On New Multiple Sclerosis Drug Targets:
The Neuroscience Research team at Children’s National Health System, under the leadership of Vittorio Gallo (who is also the Director of center and Pediatrics Professor at George Washington University School of Medicine and Health Sciences), identified novel drug targets that can reduce the rate of myelin damage along with promoting the nerve growth in MS patients. The results of this research are published in the peer reviewed journal Neuron.
Most current MS regimens are focused at prolonging the period of remission without having any influence on the growth of myelin in the brain. However, research suggests that brain cells have a limited capacity to grow and differentiate; it has been observed that cellular repair mechanisms are started years after the appearance of MS symptoms. Yet, the repair and remodeling processes remain incomplete, mainly due to unexplained factors.
Details of the Research:
As stated earlier, multiple sclerosis is marked by patchy inflammation of nerve sheaths in the brain that affect the quality of nerve transmission. However, according to the research conducted by Dr. Gallo, a newly discovered protein can help in repairing the damage caused to nervous tissue and can be used as an effective therapeutic option.
Myelin repair and regeneration (also known as remyelination) is carried out by oliogdendrocytle progenitor cells (OPCs). Prior studies indicated that most treatment strategies are only effective at improving the course of illness in patients with relapsing and remitting course but have little effect on chronic variety of MS. The same is true for OPC mediated remyelination in chronic MS.
It was observed that a naturally occurring protein Endothelin-1 (ET-1) is responsible for inhibiting the natural repair of myelin by OPC cells after injury or damage. However, any pharmacological preparation or genetic alteration that can stop the functioning of Endothelin-1 (ET-1) can enable nerve repair in MS patients. Gallo explained that ET-1 is a potential target that can be used to control remyelination in MS patients.
Given the fact that remyelination has quickly become the new vanguard for Multiple Sclerosis treatment — particularly among those with progressive forms of the disease, such as Secondary Progressive MS — these new findings will help spur new drug discoveries for future therapies.