New research reveals the importance of a protein for promoting replacement of oligodendrocytes – the specialized cells that produce myelin. The findings could have important implications for the ongoing effort to develop new and improved therapies for the treatment of demyelinating diseases.

The neurons of the brain are protected by an insulating layer called myelin. In certain diseases, such as multiple sclerosis, this protective layer is damaged and lost, leading to death of neurons and disability. 

In experiments conducted in mice by researchers at the Department of Neuroscience, at the University of Connecticut, deleting the gene that codes for the protein C1QL1 caused a delay in the rate at which the cells that make myelin (oligodendrocytes) mature, leading to reduced myelination of neurons. After mice were fed a drug that destroys myelin, recovery of oligodendrocytes and myelination were delayed in mice lacking C1QL1. Causing mice to express more C1QL1, however, led to increased numbers of oligodendrocytes and more myelination upon drug withdrawal. This suggests C1QL1 helps restore the damaged myelin layer. Thus, investigational therapies that boost C1QL1 may hold promise against demyelinating diseases.

Results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment. However, researchers said that while basic research on C1QL1 is new, there is potential for its relevancy as a novel treatment for MS. New drug treatment options for people with MS could have a large effect on their quality of life.

The findings were published in the FEBS Journal.