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Stem Cells Act Through Multiple Mechanisms To Benefit Mice With Neurodegenerative Disease [3/11/2007]

Adapted from the Burnham Institute

Human embryonic stem cells hold great promise for benefiting degenerative diseases, and do so by invoking multiple mechanisms. Such cells can be grown in a manner compatible with clinical use (i.e., without animal feeder layers) and even without the need for suppressing the immune system. These were a few of a number of conclusions arrived at by an international collaboration led by Evan Y. Snyder, M.D., Ph.D., and spearheaded by a member of his lab, Jean-Pyo Lee, Ph.D., of the Burnham Institute for Medical Research ("Burnham"). The study, to be published in Nature Medicine, was made available by advanced publication at the journal's website on March 11, 2007.

To determine whether stem cell biology might play a role in benefiting degenerative diseases, the investigators first chose to approach, as proof-of-concept, a mouse model of a representative lethal neurodegenerative disease. Next, they used mouse neural stem cells a type of "adult" stem cell, to establish the parameters of what might or might not be achievable in this disease. Then, having demonstrated success with mouse cells, they extended those insights to stem cells of human origin, both human neural stem cells and human embryonic stem cells, and, in fact, had the opportunity, for the first time, to compare those two types of controversial stem cells head-to-head in the same model. The results, described in more detail below, in fact prove to be the first successful use of human embryonic stem cells in treating a degenerative disease, significantly preserving function and extending life.

The mouse model chosen falls in a class of genetic diseases that afflicts 1 in 5000 patients, typically children (called lysosomal storage diseases), but which is often used to model an array of adult neurodegenerative diseases such as Parkinson's, amyotrophic lateral sclerosis (ALS), and Alzheimer's—particularly those with a genetic component. The mouse used here has mutation in a gene that makes the housekeeping enzyme hexosaminidase ("hex") deficient and, therefore, has Sandhoff's disease, a lethal genetic disease related to Tay-Sachs disease. When stem cells were implanted—at simply one time point—into brains of newborn mice with Sandhoff’s disease, the onset of symptoms was delayed, well-being and motor function was preserved, and lifespan was extended by greater than 70%.

The researchers discovered that their implanted neural stem cells, which migrated and integrated extensively throughout the brain, did much more than replace brain tissue destroyed by the disease. Some of the transplanted cells replaced damaged nerve cells and transmitted nerve impulses, offering the first evidence that stem cell-derived nerve cells may integrate electrically and functionally into a diseased brain. The transplanted cells also boosted the brain's supply of the enzyme Hex, which reduced the lipid accumulations in the treated animals. The experimental treatment also dampened the inflammation that typically occurs in the brains of most degenerative diseases, including Sandhoff's, and likely contributes to disease progression.

Dr. Snyder, director of Stem Cells and Regeneration at Burnham said, "…our study offers the first evidence that stem cells employ multiple mechanisms—not just cell replacement—which collaborate to benefit disease."

The researchers then sought to extend their insights to the use of human stem cells—either stem cells turned into neural progenitors from human embryonic stem cells—or isolated directly from the nervous system (called "adult" stem cells to distinguish them from embryonic stem cells even though they are taken from developing brain tissue). Both types of human stem cells were actually somewhat more effective than the mouse neural stem cells. And, they were equally as good as each other - in the first head-to-head comparison ever done between embryonic and "adult" stem cells, although the embryonic stem cells were somewhat easier to "scale up" into large quantities. Both types of human stem cells invoked the same range of multiple, collaborative mechanisms. Neither type of human stem cell created tumors, deformation, a worsening of symptoms, nor gave rise to inappropriate cells types. Neither cell type was rejected by the immune system. In fact, no suppression of the immune system was needed at all. Finally, the human embryonic stem cells were grown without mouse feeder layers and in a "defined" culture medium that is compatible with clinical use and demonstrating for the first time that such preparations are consistent with a therapeutic impact.

Currently there is no treatment for Sandhoff or Tay-Sachs. Given that the human stem cells used in this study—both human neural and embryonic stem cells—were safe and effective in so many mice, the researchers believe that their study may serve as a springboard for development into a clinical trial.

These diseases are part of a much more common group of diseases called "neurogenetic diseases." These findings contribute fundamental basic knowledge about stem cell biology that will help inform medical scientists in their quest for understanding diseases such as Parkinson's, Alzheimer's, ALS, and a host of other neurological diseases.

The Stem Cell Research Foundation is proud to have Dr. Snyder as a member of its Scientific Review Committee
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