According to a story from McGill University, researchers from the school, partnered with scientists at the University of Alberta, have unearthed a new discovery that could lead to new therapies for the treatment of multiple sclerosis.
Multiple sclerosis (MS) is a condition in which the myelin sheath, a protective, insulating cover that surrounds neurons, is damaged. Damage to the myelin sheath disrupts the ability of the cells to send electrical signals. This disruption can lead to a variety of symptoms, such as poor movement and coordination, blindness in one eye, muscle weakness, changes to sensation, fatigue, chronic pain, problems with speaking and swallowing, and mood instability and depression. While the causes of the condition are unclear, the most accepted theory is that it is an autoimmune disease in which the body’s own immune system attacks the myelin sheath. Click here to learn more about multiple sclerosis.
The researchers began the study by examining donated brain tissue from people with multiple sclerosis. Before long it became apparent that the brains of people with MS were different from normal brains because they had an unusually high concentration of the protein calnexin. This information came as a surprise to the research team. Using a mouse model of the disease, it became clear that mice without the calnexin protein were not affected by MS. Calnexin could represent another piece of the puzzle when it comes to understanding the causes of the disease. According to Marek Michalak, a professor from the University of Alberta, the protein is responsible for controlling the blood-brain barrier, and when there is too much of it, the protein allows for immune system T-cells to cross and attack neurons.
While it is clear that calnexin plays a role in MS, more research must be conducted in order to further understand more precisely how the protein is involved in regulating the blood-brain barrier. Once this is achieved, then the path to new treatment options could be opened. If there were a way to act on the functional mechanism of calnexin, it could allow for the development of therapies that could make patients resistant to multiple sclerosis.
