More than 2.3 million people worldwide are living with multiple sclerosis, a debilitating condition triggered by damage to nerve cells in the central nervous system. But in a new study published in the Annals of Clinical and Translational Neurology, researchers say they may have found a way to reduce this nerve cell damage, paving the way for new treatments for the disease.
Multiple sclerosis (MS) is a progressive neurological disease most commonly diagnosed between the ages of 20 and 50.
While the exact cause of the condition is unclear, it is known to be triggered by an autoimmune response that causes inflammation in the central nervous system. This inflammation destroys a fatty substance that protects the nerve fibers, called myelin, which causes damage to nerve cells, nerve fibers and the cells that produce myelin, called oligodendrocytes.
As a result, patients with MS can experience a broad range of symptoms, including fatigue, visual problems, muscle weakness, pain, tremors and problems with coordination and balance.
There is currently no cure for MS, though some medications are available that can alleviate symptoms and slow disease progression by targeting the body’s immune response.
But in this latest research, lead author Dr. Fang Liu, senior scientist at the Centre for Addiction and Mental Health (CAMH) in Toronto, Canada, and colleagues say they may have identified a new biological target for MS treatment.
By analyzing spinal cord tissues from deceased MS patients and animal models of the disease, the researchers identified a spinal cord alteration involving a protein that binds to a specific cell receptor associated with glutamate – the most prominent neurotransmitter in the human brain.
The team found that, compared with healthy controls, the spinal cord alteration involving this glutamate-associated protein was present at higher levels in MS animal models and deceased MS patients.
Next, the team developed a new peptide with the aim of using it to disrupt the spinal cord alteration in MS animal models.
They found that the newly created peptide effectively stopped the previously identified protein binding to the glutamate receptor, which improved neurological functioning in the animal models of MS. They found the peptide reduced nerve cell death by protecting myelin from damage, and it also improved survival of myelin-producing cells.
Dr. Liu notes that although many drugs that target glutamate receptors interfere with nerve cell signaling in the brain, the newly created peptide did not appear to have this effect, nor did it directly suppress the immune system.
Commenting on the team’s findings, she says:
“We’ve identified a new biological target for MS therapy. Our priority now would be to extend this research and determine how this discovery can be translated into treatment for patients.”
Earlier this month, Medical News Today reported on a study published in The Lancet Neurology, in which researchers claim to have mapped the complete pathological progress of MS for the first time.