Stem Cell Transplant Shows Promise Against ALS

It slowed disease progression in rats, scientists say

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MONDAY, Oct. 16, 2006 (HealthDay News) -- New stem cell research in rats may lead to treatments that slow amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease.

Grafting human stem cells into the lower spine of rats bred to duplicate the neurological illness delayed the start of nerve cell damage associated with the disease and slightly prolonged the life of the rats, say scientists at Johns Hopkins University, Baltimore.

The stem cells developed into nerve cells and created extensive connections with existing nerve cells in the rats' spines. The transplanted stem cells did not succumb to ALS, the Hopkins team found. The study was published in this week's issue of the journal Transplantation.

"We were extremely surprised to see that the grafted stem cells were not negatively affected by the degenerating cells around them, as many feared introducing healthy cells into a diseased environment would only kill them," researcher Dr. Vassilis Koliatsos, associate professor of pathology and neurosciences, said in a prepared statement.

All the rats in this study did eventually die of ALS. However, the results provide "proof of principle" for stem-cell grafts, Koliatsos said.

In the next phase of this research, his team plans to graft stem cells along the full length of the rats' spines to study the effect of the intervention on nerves and muscles in the rodents' upper body.

In the current study, Koliatsos and his colleagues, "only injected cells in the lower spine, affecting only the nerves and muscles below the waist. The nerves and muscles above the waist, especially those in the chest responsible for breathing, were not helped by these transplanted stem cells."

Much more research needs to be done before there's any possibility of using this technique in humans, Koliatsos added.

More information

The Muscular Dystrophy Association has more about ALS.

SOURCE: Johns Hopkins Medicine, news release, Oct. 16, 2006


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