Although a cure for multiple sclerosis isn't necessarily right around the corner, we may at least be getting closer to one. Scientists at Canada's University of Alberta and McGill University have zeroed in on a protein that could be a target for treatment of the disease.
The researchers started by examining donated brain tissue, some of it from people with MS, and some of it from people without. What they discovered was that the human brain endothelial cells of people with MS had much higher levels of a protein known as calnexin.
This led the scientists to take lab mice that were genetically modified to lack calnexin, and test them for susceptibility to a mouse-version of human MS. The mice were completely resistant to it, unlike a control group in which the protein was present. Why was this the case?
First of all, you need to understand how the damage caused by MS occurs. It happens when white blood cells known as T cells enter the brain and attack myelin, which is a fatty tissue that covers the fibers between nerve cells. Myelin acts kind of like the insulation on electrical wiring, so when it's compromised, the nerve cells have difficulty communicating, and neurological problems result.
"It turns out that calnexin is somehow involved in controlling the function of the blood-brain barrier," says the U of A's Prof. Marek Michalak. "This structure usually acts like a wall and restricts the passage of cells and substances from the blood into the brain. When there is too much calnexin, this wall gives angry T-cells access to the brain where they destroy myelin."
"Our challenge now is to tease out exactly how this protein works in the cells involved in making up the blood-brain barrier," adds McGill's Prof. Luis Agellon. "If we knew exactly what calnexin does in this process, then we could find a way to manipulate its function to promote resistance for developing MS."
A paper on the research was recently published in the journal JCI Insight.
Source: McGill University
Want a cleaner, faster loading and ad free reading experience?
Try New Atlas Plus. Learn more