MULTIPLE SCIEROSIS: A NEW YEAR ON THE ROLE OF INNATE IMMUNITY
Multiple Sclerosis (MS) is an inflammatory disease that leads to degradation of nerve communications in the brain and spinal cord. One of the key features of MS is the loss of the protective coating called myelin on nerve fibers. As part of its function, myelin helps to speed the transmission of electrical impulses along the nerve fiber (axon), so that loss of myelin from the nerve fiber in MS results in delayed and disjointed signals from one nerve cell to another. To put his in context, it’s like talking into a phone and having a delay between when you speak and when you hear your voice in the phone. It becomes difficult to coordinate your words and you often stumble to construct your sentences. This same type of challenge occurs in the communications between the brain and the limbs of MS patients, resulting in difficulty coordinating movements. As the myelin erodes further, so does the communication circuit.
It has been known for some time that the degradation of myelin in MS results from a misdirected immune response. Although the exact cause of the initial misdirection in MS is not yet known, the effects can be largely reproduced in animals that develop an immune response to their own myelin. This has led to the discovery and development of several drugs directed toward the adaptive immune (antibody-driven) response that have improved the standard of care for MS patients for the past 20 years, delaying recurrence of symptoms and disease progression. However, the goal of reversing the course of the disease, that is rebuilding the myelin, has remained elusive.
Recent evidence indicates a larger role for the innate immune system in MS than previously appreciated, particularly in driving degradation of myelin and progression of disease. Celtaxsys is committed to using its unique perspective and special capabilities in modulating innate immunity to create improved treatments for MS with the hope that this approach can finally fulfill the promise of reversing myelin degradation and disease progression.
