Exactly why this happens is still unclear. It may be, in part, that blocking expression of the protein, SIRT1, enhances the production of cells that make the insulating myelin sheath necessary for the transmission of nerve signals. This myelin coating is damaged in autoimmune diseases such as multiple sclerosis and Guillain-Barre syndrome. Although much more research is needed, the findings suggest that it may one day be possible to induce the brains of patients with myelin-associated diseases or injuries to heal themselves by selectively interfering with the activity of SIRT1.
“We are excited by the potential implications our study has on demyelinating diseases and injuries,” said Anne Brunet, PhD, an associate professor of genetics. “It’s intriguing because activating SIRT1 is typically considered to be beneficial for metabolism and health, but in this case, inactivating SIRT1 can provide protection against a demyelinating injury.” Brunet, who is also a member of the Stanford Cancer Institute, is the senior author of the research, which was published online May 5 in Nature Cell Biology. Postdoctoral scholar Victoria Rafalski, PhD, is the lead author of the study. Blocking SIRT1 expression appears to work by promoting the development of neural stem cells in the brain into a type of cell called an oligodendrocyte precursor. These cells, in turn, become the mature oligodendrocytes that wrap the long arms of neurons with myelin—a fatty material necessary to facilitate the transmission of the electrical impulses from one nerve cell to another. In humans, most myelination occurs during infancy and adolescence. Diseases such as multiple sclerosis wreak havoc in the central nervous system by damaging this protective myelin coating and impeding communication between nerve cells.