Enzyme in Myelination Process Sheds Light on Multiple Sclerosis


Study may lead to the development of treatments for disorders with damaged myelin sheath.

When DNA methyltransferase (DNMTs) are removed during oligodendrocyte progenitor cell (OPCs) differentiation, it results in a reduced amount of myelin in nervous tissue and neurological deterioration, according to a study published in Cell Reports.

Oligodendrocytes (OLs) derive from OPCs — stem-like cells that divide and generate OLs through gene regulation.

The result of the study found that in order for OPCs to develop into myelin-forming cells, it required DNMTs. When DNMTs are added, the genes are unable to be expressed and are “silenced.”

Within the study, mice experienced significant neurological symptoms, such as tremors, loss of control of body movement, and eventual death.

“Our group has previously observed altered DNA methylation in the brain of patients with multiple sclerosis, the most devastating adult demyelinating disorder, but its role in myelin formation and the identity of the genes silenced by DNMT's in OPCs were not known,” said lead study investigator Patrizia Casaccia, MD, PhD. “A better understanding of why DNA methylation is important for myelin formation and what genes need to be shut off during the formation of OLs from OPCs has important implications not only for development, but also for myelin repair.”

These findings could lead to the development of treatments for disorders with damaged myelin sheath, as well as helping to better understand how OPCs transform into brain cancer cells.

More research still needs to be done to understand the underlying causes of aberrant DNMT in the brains of multiple sclerosis patients and in preclinical models.

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