Multiple sclerosis is an autoimmune disease that attacks the myelin cover of nerve cells from any region, in the brain, in the spinal cord and even in peripheral nerves, disrupting the process of transmitting signals. Multiple sclerosis symptoms are variated and depend on which nerve cells are affected first, but without a doubt from the central nervous system to the peripheral one it causes symptoms that highly affect daily activities and shorten life expectancy. From numbness and weakness in arms and legs to lack of coordination and thinking problems that only worsen in time every part of the body can get affected.
As the actual cause behind this autoimmune response hasn’t been found, a proper treatment doesn’t exist yet, although there are many clinical trials that focus on reducing the disease’s symptoms, thus improving the daily lives of multiple sclerosis patients. But Ph.D. Chang-Qing Xia’s research on mice with autoimmune encephalomyelitis, made at the University of Florida, promises a lot of hope for future treatments of multiple sclerosis. Although experimental autoimmune encephalomyelitis in mice isn’t identical to multiple sclerosis it is similar enough to take into consideration.
By trying out a method already used to treat autoimmune diseases, researcher Chang-Qing Xia managed to reverse the mice’s disease to early stages. He used a chemical shortly called SMCC or sulfo-SMCC, which is approved by US FDA to help bind the autoantigens of the diseases with spleen cells. This method of binding autoantigens, which are protein fragments of myelin with spleen cells using SMCC is a fast and easy process that is also less toxic to cells when used as a treatment.
M.D. Xia considers that “the most important thing is that these findings are highly translatable to the clinic,” meaning that the next step is finding a way of transforming the successful experiments into a human clinical trial. The researcher’s hypothesis is that the experimental autoimmune encephalomyelitis and multiple sclerosis are similar diseases pathologically and immunologically and by combining human protein fragments of myelin known as autoantigens with white blood cells a transfusion serum could be developed. Hopefully, the same result could be observed in multiple sclerosis, even if the damage cannot be entirely repaired, keeping the disease at an early stage or simply stopping the damaging process could mean a breakthrough for multiple sclerosis treatment.
A lot of effort has to be put into making this experiment a clinical trial, but Xia believes that his simple methods can work with multiple sclerosis which already uses approved drugs for clinical trials. With a little support we might just see a new form of multiple sclerosis treatment in the near future.