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Scientists infuse rat spinal cords with brain-derived human stem cells

nce inside the brain or spinal cord, neural progenitor cells grow into neuron-supporting stem cells called astrocytes. Some researchers believe that ALS causes astrocyte malfunction, which in turn causes motor neurons to degenerate and eventually die.

Several research groups around the world are trying to unleash the therapeutic potential of neural progenitor cells. But the UW-Madison work is the first "double whammy," says Svendsen, because the injected neural progenitor cells develop into astrocyte-like cells and simultaneously secrete glial cell-line derived neurotrophic factor (GDNF), a naturally occurring protein that preserves motor neurons during development. The twofold approach has a better chance of protecting healthy neurons that haven't already succumbed to ALS, he says.

Approximately 5,600 people in the United States are annually diagnosed with ALS. Also known as Lou Gehrig's disease, ALS is not well understood, though mutations in the SOD-1 gene -- or superoxide dismutase-1 -- are known to play a role. ALS attacks nerve cells in the brain and spinal cord, and as motor neurons progressively die, the brain can no longer initiate and control muscle movement.

The UW-Madison researchers tackled several technical barriers trying to ensure that the progenitor cells correctly gather near the motor neurons in the spinal cord, while continuing to pump GDNF once there, says Sandra Klein, lead author of the study and a UW-Madison doctoral researcher.

But making GDNF-emitting stem cells was the first puzzle to grapple with. Svendsen and his team approached the problem using a genetically engineered viral structure known as a lentivirus. Collaborating with Patrick Aebischer, a researcher in Switzerland, the scientists manipulated the lentivirus' genetic machinery, directing it to secrete GDNF. The team then infected neural progenitor cells with the GDNF-pumping lentivirus. Once the cells were infected, the scientists washed the virus away, leav
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Contact: Clive Svendsen
svendsen@waisman.wisc.edu
608-265 8668
University of Wisconsin-Madison
19-Apr-2005


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