Cell transplant may restore lost sight
http://www.newscientist.com/article.ns?id=mg19225775.100
* 08 November 2006
* NewScientist.com news service
* Becky McCall
A FEW blind mice have had their sight restored. The process, which involved transplanting precursor retinal cells into their damaged eyes, promises a cure for age-related macular degeneration or blindness due to diabetes.
The mice were blind because they had been bred to have non-functional photoreceptor cells, the eye's rod and cone cells that convert light into electrical signals to be sent to the brain. Elderly people and people with diabetes can also lose their vision when these cells fail.
In principle, restoring sight to animals that have simply lost photoreceptor cells should be relatively easy, because most of the brain's wiring for vision is still intact. Previous attempts to treat such blindness by transplanting stem cells had been unsuccessful, however. The stem cells had not developed enough to properly integrate with the recipient's retina and existing vision-related regions of the brain.
Now a team led by Robin Ali from University College London (UCL) and Robert MacLaren, an eye surgeon from Moorfields Eye Hospital, London, have overcome this problem by using retinal precursor cells that were at a later stage of development than stem cells. The team took these cells from healthy donor mice only after the cells had started producing rhodopsin, a pigment necessary for sensitivity to light. When transplanted into the eyes of blind mice, the retinal precursor cells differentiated into rod cells and grew to make the short neural connections required to restore sight. The team tested the mice's vision by observing how their pupils responded to different light intensities (Nature, vol 444, p 203).
"This research is the first to show that photoreceptor transplantation is feasible," MacLaren says. "We are now confident that this is the avenue to pursue to uncover ways of restoring vision to thousands who have lost their sight."
While this method may be workable in humans, it is not yet clear where doctors will find donor retinal precursor cells that the recipient will not reject.
One option is to grow human embryonic stem cells to the appropriate stage of development for transplantation. Earlier this year, Thomas Reh of the University of Washington in Seattle managed to do exactly this. "We can derive retina cells, including cells at exactly the stage that Ali's group found were best for transplantation, from human embryonic stem cells," says Reh. "So joining the approaches would seem to be an important next step in treating retinal degeneration and restoring vision. Stay tuned."
The UCL team also suggests the use of stem-cell-like precursor cells that are found on the edge of the retina. These cells could be harvested and transplanted into the retina if the disease is caught at an early stage in humans.
* 08 November 2006
* NewScientist.com news service
* Becky McCall
A FEW blind mice have had their sight restored. The process, which involved transplanting precursor retinal cells into their damaged eyes, promises a cure for age-related macular degeneration or blindness due to diabetes.
The mice were blind because they had been bred to have non-functional photoreceptor cells, the eye's rod and cone cells that convert light into electrical signals to be sent to the brain. Elderly people and people with diabetes can also lose their vision when these cells fail.
In principle, restoring sight to animals that have simply lost photoreceptor cells should be relatively easy, because most of the brain's wiring for vision is still intact. Previous attempts to treat such blindness by transplanting stem cells had been unsuccessful, however. The stem cells had not developed enough to properly integrate with the recipient's retina and existing vision-related regions of the brain.
Now a team led by Robin Ali from University College London (UCL) and Robert MacLaren, an eye surgeon from Moorfields Eye Hospital, London, have overcome this problem by using retinal precursor cells that were at a later stage of development than stem cells. The team took these cells from healthy donor mice only after the cells had started producing rhodopsin, a pigment necessary for sensitivity to light. When transplanted into the eyes of blind mice, the retinal precursor cells differentiated into rod cells and grew to make the short neural connections required to restore sight. The team tested the mice's vision by observing how their pupils responded to different light intensities (Nature, vol 444, p 203).
"This research is the first to show that photoreceptor transplantation is feasible," MacLaren says. "We are now confident that this is the avenue to pursue to uncover ways of restoring vision to thousands who have lost their sight."
While this method may be workable in humans, it is not yet clear where doctors will find donor retinal precursor cells that the recipient will not reject.
One option is to grow human embryonic stem cells to the appropriate stage of development for transplantation. Earlier this year, Thomas Reh of the University of Washington in Seattle managed to do exactly this. "We can derive retina cells, including cells at exactly the stage that Ali's group found were best for transplantation, from human embryonic stem cells," says Reh. "So joining the approaches would seem to be an important next step in treating retinal degeneration and restoring vision. Stay tuned."
The UCL team also suggests the use of stem-cell-like precursor cells that are found on the edge of the retina. These cells could be harvested and transplanted into the retina if the disease is caught at an early stage in humans.
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