before it's in the papers"
August 03, 2010
TO THE WORLD SCIENCE HOME PAGE
Link found between premature-aging disease, normal aging
and World Science staff
Researchers say they have found the first clear link between an “early-aging” disorder that kills children, and normal aging—boosting hopes that finding a cure for the first could help fight the second.
Researchers have long speculated that the premature-aging disorders, which can end children’s lives as soon as their early teens, were somehow accelerated versions of normal aging. If so, then studying these disorders might have a side benefit for the rest of us: giving biologists a powerful way to understand, and perhaps “treat,” ordinary aging.
But scientists previously had found no clear link between premature aging syndromes and normal aging at a detailed level, although superficial resemblances were obvious. Children with the devastating Hutchinson-Gilford Progeria Syndrome, for instance, “age” at seven times the normal rate, so a 10-year-old patient may have heart conditions and arthritis typical of a 70-year-old.
Some scientists have downplayed similarities between the syndrome and normal aging, because a detailed analysis can also reveal important differences. But in the new study, researchers linked Hutchinson-Gilford Progeria Syndrome—the most drastic premature-aging disorder—to normal aging at a molecular level.
Researchers had previously attributed the syndrome, currently incurable, to a mutation in a gene known as lamin A. The mutation leads the body to produce a defective, shortened version of a molecule by the same name that is part of the covering of the cell nucleus. Biologists are studying these defects in an effort to find treatments for the disorder.
In the new study, Paola Scaffidi and Tom Misteli of the National Cancer Institute in Bethesda, Md., found that the same defect occurs sporadically in the cells of normally aged people. These cells, they reported, share some of the aberrations that occur in cell nuclei in people with the syndrome, such as unrepaired DNA damage.
By blocking the defect in the molecules, the researchers said they were able to reverse some of the cellular defects. The finding “suggests that lamin A participates in the aging process in healthy individuals,” they wrote, and that this process is “exaggerated” in sick people.
The findings appear in the April 27 issue of the research journal Science.
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