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Yale researchers succeed in using stem cells to repair damaged spinal cord in primates

Yale University : 14 November, 2000  (New Product)
A Yale research team has transplanted stem cells from a primate to repair the protective sheath around the spinal cord in the same animal, an accomplishment that some day could help people with spinal cord injuries and multiple sclerosis.
'The concept is not ready for people, but the fact that it can be achieved in a primate is significant,' said Jeffrey Kocsis, professor of neurology and neurobiology at Yale School of Medicine. 'Cells were taken from the same animal, with minimal neurological damage, and then injected to rebuild the myelin.'

In multiple sclerosis, the immune system goes awry and attacks the myelin. Damage to the myelin builds up over years, causing muscle weakness or paralysis, fatigue, dim or blurred vision and memory loss.

Using the primate's own cells to repair the myelin, which is a fatty sheath that surrounds and insulates some nerve cells, sidesteps a common problem in transplanting organs. Patients generally have to take drugs to suppress their immune systems so that their bodies do not reject an organ obtained from a donor.

'We didn't even need to immunosuppress the primate,' said Kocsis, who presented his findings last week at the annual meeting of the Society for Neuroscience in New Orleans.

The experiment involved collecting small amounts of tissue from the subventricular area of the primate brain using ultrasonography. The neural precursor cells, or stem cells, then were isolated and expanded in vitro using mitogen, an agent that promotes cell division.

At the same time, myelin was removed from the primate's spinal cord. The stem cells were then injected in the same spot to form new myelin to cover the nerve fibers.

'The lesions were examined three weeks after transplantation and we found the demyelinated axons were remyelinated,' Kocsis said. 'These results demonstrate that autologous transplantation of neural precursor cells in the adult non-human primate can remyelinate demyelinated axons, thus suggesting the potential utility of such an approach in demyelinating lesions in humans.'
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