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Brain, heal thyself? Stanford research describes delayed onset of multiple sclerosis in mice

What if it were possible, when faced with a devastating neurological disease like multiple sclerosis, to coax the brain to heal itself? Unfortunately, we're probably still years away from any kind of quick fix for these conditions (if, in fact, one exists at all). But recent research by Stanford geneticist Anne Brunet, PhD, describes an intriguing way to delay the onset of a multiple-sclerosis-like disease in laboratory mice. The study is published in the most recent issue of Nature Cell Biology.

We're excited by the potential implications our study has on demyelinating diseases and injuries

Specifically, the researchers created a type of mouse in which they could turn the expression of a protein called SIRT1 on and off in the neural stem cells in the animals' brains. (They wanted to investigate SIRT1's involvement in the disease because it appears to be highly expressed in the brains of mice with multiple sclerosis.) They found that animals in which the protein's expression was blocked developed the characteristic paralysis of the disorder more slowly than their peers with normal levels of SIRT1 expression.

From our article:

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.

Brunet, who last year received a Pioneer Award from the National Institutes of Health for her work in studying the inheritance of longevity, worked with Stanford neurologist and noted multiple sclerosis researcher Lawrence Steinman, MD, to conduct the study. She told me:

We are excited by the potential implications our study has on demyelinating diseases and injuries... 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.

Previously: NIH awards nine Stanford faculty funding for innovative research, Black hat in Alzheimer's, white hat in multiple sclerosis? and Amyloid, schmamaloid: Stanford MS expert finds dreaded proteins may not be all bad.

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