Researchers with the University of Virginia School of Medicine have shown that a type of cell called oligodendrocyte progenitor cells play a significant role in the development of MS.
Multiple sclerosis, or MS, is an unpredictable disease of the central nervous system. In it, the body’s immune system attacks the myelin, which is an insulating layer around nerve cells. It leads to progressive neurological symptoms, including visual problems, tingling and numbness, pain, spasms, fatigue, weakness, balance problems, and can lead to cognitive issues and other severe symptoms.
Researchers with the University of Virginia School of Medicine have shown that a type of cell called oligodendrocyte progenitor cells (OPCs) play a significant role in the development of MS. These cells had largely been ignored, with many believing the cells could only play a positive role in MS. These glial cells make up approximately 5% of the brain and spinal cord and their job is to make cells that produce myelin.
It was thought that in MS the oligodendrocyte progenitor cells aren’t efficient enough in creating myelin-producing cells. However, the UVA researchers found instead that the cells actively participate in the immune system attacks on myelin.
“This cell type is modulating the inflammatory environment,” said Anthony Fernandez-Castaneda, graduate student and first author of the study. “I was very surprised that these progenitor cells, thought to be a bystander during the inflammatory process, are active contributors to neuroinflammation.”
The research was published the journal Acta Neuropathologica.
The researcher team, led by UVA’s Alban Gaultier, generated an oligodendroglia-specific knockout of the low-density lipoprotein receptor-related protein 1 (LRP1), which is a phagocytic receptor highly expressed in several types of CNS cells, including OPCs. The laboratory animals that lacked LRP1 in OPCs had a significant decrease in inflammation processes. The research team concluded that OPCs play a major role in regulation of neuroinflammation in an LRP1-dependent fashion.
Neuroinflammation is also increasingly being connected to the cognitive and memory damage found in Alzheimer’s patients.
“In MS, we have many ways to modulate the initial immune attacks, but we really have no way to promote brain repair,” said Gaultier. “To come up with a cure, we have to target both aspects of the pathology.”
Which will be difficult, because the OPCs play several major roles. Any therapies developed can’t just shut OPCs down.
“It’s going to take a lot more work to translate these findings to any form of therapy,” Gaultier added. “We are shining the light on this cell type that very few people have studied as part of the inflammatory response in the brain. More consideration should be given to the varied roles the progenitor cells play when focusing on finding a cure for MS.”
Multiple sclerosis affects about 2 million people worldwide. It is the most common neurological disease in the young, often diagnosed between the age of 20 and 50. It is estimated that 8,000 to 10,000 children under the age of 18 live with MS and it has also been seen to develop in individuals as old as 75.
The causes of MS are largely unknown. Many scientists believe it is triggered by one or more environmental factors in genetically susceptible individuals, while other researchers believe it is an autoimmune disease. However, because a specific target of the immune attack hasn’t been identified, it is generally referred to as an immune-mediated disease. Women are more likely than men to development MS. There is no evidence it is directly inherited, but certain genetic factors appear to increase susceptibility.
