The absence of epigenetic factors in myelin-producing oligodendrocyte cells make sure that myelin production is switched off in the adult brain. Targeting these factors may be a way of triggering myelin regeneration in multiple sclerosis (MS), and a step toward personalized medicine for this disease, Dr. Patrizia Casaccia said in a talk at the ACTRIMS 2017 Forum.
Casaccia is a professor of neuroscience and neurology at the Icahn School of Medicine at Mount Sinai in New York with considerable experience in myelination research. Recently, she and her team found that oligodendrocytes (cells that produce myelin) use epigenetic mechanisms to switch off genes necessary for myelination when not needed.
Epigenetics is a means for cells to control which genes are active. Since all cells share the same DNA, gene activity — resulting from switching genes on and off — determines how each cell looks and works. Epigenetics involves the placement of chemical tags on the DNA that, for instance, tell the protein-making machinery whether the gene should remain silent.
During development, genes that prevent myelin formation are inactivated with the help of epigenetic tags — allowing the production of myelin. When the myelin sheath is damaged, this developmental process starts again, with epigenetic factors blocking the suppressor genes and so promote myelin growth.
But, according to Casaccia, the ability of the epigenetic silencing mechanism to activate myelin production is lost as we age. Her team is now exploring ways of getting rid of these suppressor genes.
Interestingly, research from her lab showed that social experiences and external stimuli can impact epigenetic mechanisms in oligodendrocytes, and so alter gene activity.
Since epigenetic factors are influenced by the environment, she suggests that specific symptoms of MS, as well as the disease’s course, result from a combined impact of genes and environmental factors — including sun exposure and gut bacteria — that act via epigenetics to change gene expression.
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