An autoimmue disease results when the immune system attacks the body’s own tissues. MS is a serious condition in which nerve-cell projections, or axons, in the brain and the spinal cord are destroyed as a result of misdirected inflammatory reactions. It is often characterized by an unpredictable course, with periods of remission being interrupted by episodes of relapse.
It is commonly thought that the primary target of MS is the myelin sheath, a membrane surrounding axons that increases the speed of a nerve signal. However, damage to nerve fibers is also a central process.
A team of researchers led by LMU Munich Professor Martin Kerschensteiner of the Medical Center of the University of Munich and Professor Thomas Misgeld from the Technical University of Munich has now been able to explain how the damage is inflicted. Their results show that the inflammatory reaction can induce a previously unknown type of axonal degeneration, which they call "focal axonal degeneration" (FAD). In an animal model of MS, this process is reversible if it is recognized and treated early, so the researchers believe that it could serve as a potential target for therapeutic intervention.
Instead FAD is responsible for the primary damage. FAD can damage axons that are still wrapped in their protective myelin sheath. This process could also help explain some of the spontaneous remissions of symptoms that are characteristic of MS. "In its early stages, axonal damage is spontaneously reversible," Kerschensteiner was quoted as saying. "This finding gives us a better understanding of the disease, but it may also point to a new route to therapy, as processes that are in principle reversible should be more susceptible to treatment."
"In our animal model, at least, we can neutralize these radicals and this allows acutely damaged axons to recover," Kerschensteiner said. The characteristic signs of the newly discovered process of degeneration can also be identified in brain tissue from patients with MS, suggesting that the basic principle of treatment used in the mouse model might also be effective in humans.
"Before appropriate therapeutic strategies can be developed, we need to clarify exactly how the damage arises at the molecular level," Kerschensteiner said. "We also want to investigate whether similar mechanisms play a role in later chronic stages of multiple sclerosis."
SOURCE: Nature Medicine, published online March 27, 2011