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Stanford: treatment delays multiple sclerosis onset in mice

Researchers from the Stanford University School of Medicine discovered that blocking the expression of a single protein in the brains of mice with a form of multiple sclerosis can delay its effects, including paralysis.

The protein, SIRT1, helps to produce the cells that make the protective myelin coating needed to transmit nerve signals in the brain. Autoimmune diseases such as multiple sclerosis damage this coating, impeding communication between nerve cells.

"We are excited by the potential implications our study has on demyelinating diseases and injuries," said Anne Brunet, associate professor of genetics at Stanford and the senior author of the research. "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."

The process works by developing neural stem cells in the brain into another type of cell, called an oligodendrocyte precursors. Mature oligodendrocytes wrap neurons' arms with protective myelin, helping transmit electrical impulses from one cell to another.

Brunet and her team began by injecting a lab mouse with a drug called tamoxifen, which can effectively turn the SIRT1 gene off in neural stem cells.

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Over time, nerve stem cells in which SIRT1 expression had been blocked began to make proteins that looked like typical oligodendrocyte precursor cells. The lack of SIRT1 activity increased the production of cells that express oligodendrocyte-specific protein makers.

When the researchers injected normal mice and those with blocked SIRT1 expression with a compound that causes the demyelination of nerve cells just as multiple sclerosis does, the SIRT1-blocked mice had quicker recoveries than the normal mice. They were also protected for a time from the paralysis that comes after the onset of multiple sclerosis.

"Our study highlights the possibility of pharmacological manipulation of multiple nodes of the pathway to expand the population of oligodendrocyte precursors," Brunet said. "Approaches such as these could have important implications for regenerative medicine."

The research was published online May 5 in Nature Cell Biology, a journal that publishes cell-related research and papers.

The research was supported by the California Institute for Regenerative Medicine, the National Institutes of Health, a grant from the American Federation for Aging Research, a National Brain Tumor Society grant, the Glenn Foundation for Medical Research, the National Science Foundation, the Guthy-Jackson Charitable Foundation and the National Multiple Sclerosis Society.

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Stanford: treatment delays multiple sclerosis onset in mice

Uploaded: Mon, May 13, 2013, 9:50 am

Researchers from the Stanford University School of Medicine discovered that blocking the expression of a single protein in the brains of mice with a form of multiple sclerosis can delay its effects, including paralysis.

The protein, SIRT1, helps to produce the cells that make the protective myelin coating needed to transmit nerve signals in the brain. Autoimmune diseases such as multiple sclerosis damage this coating, impeding communication between nerve cells.

"We are excited by the potential implications our study has on demyelinating diseases and injuries," said Anne Brunet, associate professor of genetics at Stanford and the senior author of the research. "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."

The process works by developing neural stem cells in the brain into another type of cell, called an oligodendrocyte precursors. Mature oligodendrocytes wrap neurons' arms with protective myelin, helping transmit electrical impulses from one cell to another.

Brunet and her team began by injecting a lab mouse with a drug called tamoxifen, which can effectively turn the SIRT1 gene off in neural stem cells.

Over time, nerve stem cells in which SIRT1 expression had been blocked began to make proteins that looked like typical oligodendrocyte precursor cells. The lack of SIRT1 activity increased the production of cells that express oligodendrocyte-specific protein makers.

When the researchers injected normal mice and those with blocked SIRT1 expression with a compound that causes the demyelination of nerve cells just as multiple sclerosis does, the SIRT1-blocked mice had quicker recoveries than the normal mice. They were also protected for a time from the paralysis that comes after the onset of multiple sclerosis.

"Our study highlights the possibility of pharmacological manipulation of multiple nodes of the pathway to expand the population of oligodendrocyte precursors," Brunet said. "Approaches such as these could have important implications for regenerative medicine."

The research was published online May 5 in Nature Cell Biology, a journal that publishes cell-related research and papers.

The research was supported by the California Institute for Regenerative Medicine, the National Institutes of Health, a grant from the American Federation for Aging Research, a National Brain Tumor Society grant, the Glenn Foundation for Medical Research, the National Science Foundation, the Guthy-Jackson Charitable Foundation and the National Multiple Sclerosis Society.

— Elena Kadvany

Comments

Jon
Evergreen Park
on May 13, 2013 at 10:50 am
Jon, Evergreen Park
on May 13, 2013 at 10:50 am

I wonder if this research also applies to peripheral neuropathy, where nerves in the arms and legs gradually lose their ability to transmit impulses.


Lourdes Water
Another Palo Alto neighborhood
on May 13, 2013 at 6:50 pm
Lourdes Water, Another Palo Alto neighborhood
on May 13, 2013 at 6:50 pm

OMG! This is such good news. I was recently diagnosed with a peripheral neuropathy similar to MS, called CIDP ( chronic immunological Demyelinating neuropathy) , which is an imitator of MS, also. many of the very expensive treatments are the same. They are both Autoimmune diseases.

Remyelination of the nerve sheath is slow and touchy, and the autoimmune disease will often eat the new myelin right off the nerves, then causing scarring which complicates matters and prevents healing. Those are the plagues seen in MS

This is indeed good news for me, as I need to be up and running for my tiny grandchildren who need me so. I am overjoyed! Merci, gracias, vielen danke!


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