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For the more than 30,000 people worldwide who suffer spinal-cord injuries each year, research by a postdoctoral fellow at MIT’s Picower Institute for Learning and Memory could one day result in some very good news.

When spinal injury results in paralysis, the cause is usually damage to nerve-cell axons, the long fibers that conduct electrical impulses to and from the brain. Damaged axons either don’t regenerate themselves or remain deficient in myelin, the sheath that protects them and allows them to transmit signals quickly and reliably. Research published in the July issue of PLoS Biology by the Picower Institute’s Konstantinos Meletis and colleagues at the Karolinska Institute in Sweden suggests that stem cells in the spinal cord itself could help repair that damage.

In several past studies, other researchers have grown stem cells in vitro from cells taken from adult spinal cords. To study how neural stem cells operate in vivo, Meletis and his colleagues identified a population of mouse spinal-cord cells that they suspected had the potential to display stem-cell characteristics. Then they genetically engineered mice to mark those cells with green fluorescent protein. “We could then see both the initial stem-cell population and the type of cells they give rise to after spinal-cord injury,” Meletis says.

They found that after a spinal-cord injury, the stem cells proliferated and migrated toward the injury site, where they differentiated into two cell types. The majority became scar-forming cells, but a small population became a valuable type of cell called an oligo­dendrocyte, which has the ability to wrap around axons and form myelin. “Oligodendrocytes are thought to be important for repairing spinal-cord injury,” says Meletis. The researchers hope that their work could lead to therapies that encourage an injured spinal cord’s own stem cells to ramp up production of oligodendrocytes and minimize the production of scar-forming glia, which inhibit regeneration. With more oligodendrocytes around to form more myelin, axons would stand a better chance of getting back to work transmitting signals to and from the brain.

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Credit: Design by Marie Carlén, confocal image by Fanie Barnabé-Heider

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