The neurons of the brain are protected by an insulating layer called myelin. In certain diseases like multiple sclerosis, this protective layer is damaged and lost, leading to death of neurons and disability. New research published in The FEBS Journal reveals the importance of a protein called C1QL1 for promoting the replacement of 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.
In experiments conducted in mice, deleting the gene that codes for C1QL1 caused a delay in the rate at which oligodendrocytes (the cells that make myelin) 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 the C1QL1 protein. Causing mice to express more C1QL1, however, led to increased numbers of oligodendrocytes and more myelination upon drug withdrawal, suggesting that C1QL1 helps to restore the damaged myelin layer. Thus, investigational therapies that boost C1QL1 may hold promise against demyelinating diseases.
“Our basic research on C1QL1 is nascent, but there is potential that it is relevant for a novel treatment for multiple sclerosis,” said corresponding author David C. Martinelli, PhD, of the University of Connecticut Health Center. “New drug treatment options for patients with multiple sclerosis could have a large impact on their quality of life.”
URL: https://onlinelibrary.wiley.com/doi/10.1111/febs.17256
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