Friday, December 21, 2012

Neural stem cells show signs of treating ALS (Lou Gehrig's disease) in mice

A consortium of researchers around the U.S. used transplanted neural stem cells (shown here) to treat a mouse model of ALS.
CIRM grantees at Sanford-Burnham were part of a consortium that found transplanted neural stem cells slows the progress of a form of Lou Gehrig’s disease (amyotrophic lateral sclerosis or ALS) in mice.

It’s still too early to celebrate – mice are quite different than humans, and treating a disease in one doesn’t necessarily translate into a therapy for the other – but it’s nice to see signs of hope for a disease that’s desperately in need of a therapy. ALS is a fatal disease in which the nerve cells that control movement die.

Sanford-Burnham described the study, which was published in Science Translational Medicine, on their blog:
In this study, researchers at multiple institutions conducted 11 independent studies to test neural stem cell transplantation in a well-established mouse model of ALS. They all found that this cell therapy reduced the symptoms and course of the ALS-like disease. They observed improved motor performance and respiratory function in treated mice. Neural stem cell transplant also slowed the disease’s progression. What’s more, 25 percent of the treated ALS mice in this study survived for one year or more—roughly three to four times longer than untreated mice.
They went on to describe how the cells helped slow the disease:
Transplanted neural stem cells helped the ALS mice, but not for the obvious reason—not because they became nerve cells, replacing those missing in the ALS spinal cord. The biggest impact actually came from a series of other beneficial neural stem cell activities. It turns out neural stem cells produce protective molecules. They also trigger host cells to produce their own protective molecules. In turn, these factors help spare host nerve cells from further destruction.
We have more information on our website about our stem cell funding for ALS.

A.A.

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