Multiple Sclerosis Treatment
Researchers at Stanford University Medical Center have made new advances in the treatment of multiple sclerosis. Experiments conducted on laboratory animals have shown that blocking the expression of the protein, SIRT1, delays the onset of paralysis on multiple sclerosis. Multiple sclerosis is a neurodegenerative disease characterized by demyelination of the nervous system, leading to a wide range of neurological signs and symptoms. Anne Brunet, PhD, an associate professor of genetics, says they are excited about the potential this finding has in the treatment of neurodegenerative diseases. “Our study highlights the possibility of pharmacological manipulation of multiple nodes of the pathway to expand the population of oligodendrocyte precursors,” said Brunet.
However it is not known the exact mechanism by which blocking SIRT1 protein delays paralysis in multiple sclerosis. One possible explanation would be that by blocking this protein it is stimulated the production of insulating myelin sheath that is required for nerve transmission. Dr Brunet said that their discovery is intriguing because activation of SIRT1 is considered beneficial for health and in this case inactivation of SIRT1 protects against demyelination. Although other studies are needed in this direction, researchers are optimistic that someday patients with multiple sclerosis symptoms will be alleviated by interfering SIRT1 protein in the brain.
It seems that blocking SIRT1 leads to the transformation of neural stem cells into oligodendrocyte precursors, which is a type of brain cell. These precursors are transformed into mature cells, that is oligodendrocytes, which help myelination of axons. It should be noted that myelin is composed of lipid material and has an essential role in nerve transmission. Multiple sclerosis means diffuse demyelination of neurons and this can lead to a range of symptoms such as optic neuritis (impaired vision), motor deficits, paresthesia, diplopia (double vision), ataxia, vertigo, etc..
Brunet and her colleagues conducted several experiments on laboratory animals and found that by turning off the expression of SIRT1 in mice, the production of oligodendrocytes increased. Furthermore, when the researchers injected a compound that caused demyelination in both healthy mice and in those with inhibited SIRT1 expression, it was found that the latter recovered faster. To understand more about how work SIRT1 works in the brain, researchers searched and identified a number of genes that were expressed more intensely when SIRT1 is inhibited. These genes are related to cell metabolism, growth factor signaling and protein production. It seems that one of them, PDGFRalpha, is associated with the production of oligodendrocytes and inactivation of SIRT1.