Researchers say they have uncovered a mechanism behind the normal aging process, based on studies of children with a devastating “early-aging” disorder.

Many scientists have speculated that certain premature-aging disorders, which can end children’s lives by their early teens, are somehow accelerated versions of normal aging.

If so, then studying these conditions 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 trouble finding clear links, at a detailed level, between these syndromes and normal aging.

Superficial resemblances were obvious. For instance, children with the devastating Hutchinson-Gilford Progeria Syndrome “age” at seven times the normal rate, so a 10-year-old patient could have heart conditions and arthritis typical of a 70-year-old.

But some scientists have downplayed the similarities to normal aging, because detailed analyses also reveal important differences.

Nonetheless, in the new study, researchers linked Hutchinson-Gilford Progeria—the most drastic of the major premature-aging disorders—to normal aging, at a molecular level.

Scientists 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 the abnormality 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 abnormalities. The finding “suggests that lamin A participates in the aging process in healthy individuals,” they wrote, and that this process is “exaggerated” in the sick people.

Thus, “this is a novel potential mechanism involved in aging,” Misteli wrote in an email. The findings appear in the April 27 issue of the research journal Science.

ABOUT THE AUTHOR

Science writer Jack Lucentini is founder and editor of the World Science science news webzine. He has worked as a staff writer at three daily newspapers, and as a freelance science writer for a range of publications including The Washington Post, Discover magazine and The Scientist magazine. He earned his bachelor's degree at Oberlin College in Oberlin, Ohio in 1993.