A molecule that helps blood clot may also play a role in multiple sclerosis relapses, research report in the May 6 issue of PNAS. The new research may help answer the mystery of why remissions happen, as well as find early markers of the disease.
The research also shows a new way to study multiple sclerosis (MS) in mice that is closer to the human form of the disease.
MS affects about a million people in the United States and many more globally. It damages the brain’s ability to communicate with the rest of the body, making it hard to walk, write, or hold a fork and knife. This happens because of damage to the insulation around the nerves. Just like a frayed wire, a nerve with damaged insulation can short out or send bad signals.
But the damage isn’t permanent, at least not at first. Most people with multiple sclerosis have recurring episodes of disability, followed by remissions when their symptoms lessen or disappear.
Why these relapses and remissions happen is a great mystery. We know that the damage to the nerves is caused by immune system, the army of cells in our body that is supposed to protect us from disease-causing invaders. For some reason, in MS, the immune system turns on cells in the brain and spinal cord. In MS patients, a particular type of immune cell – CD8+cells, a part of the immune system that normally kills cells that are cancerous or infected – seem to be he ones doing the damage.
Although researchers have been able to develop drugs to help fight MS using a mouse version of MS, these experimental mice develop a slightly different immune system response that what happens in MS in humans. Different cells do the damage in MS mice: CD4+ cells. The mice have CD8+ cells, but those CD8+ cells are generally quiescent. This has been a big stumbling block to understanding how the immune system develops in MS.