Stanford, Calif. - We can dye gray hair, lift sagging skin or boost lost hearing, but no visit to the day spa would be able to hide a newly discovered genetic marker for the toll that time takes on our cells. "We've found something that is at the core of aging," said Stuart Kim, PhD, professor of developmental biology and of genetics at the Stanford University School of Medicine.
In a study to be published in the July 21 issue of Public Library of Science-Genetics, Kim and colleagues report finding a group of genes that are consistently less active in older animals across a variety of species. The activity of these genes proved to be a consistent indicator of how far a cell had progressed toward its eventual demise.
Until now, researchers have studied genes that underlie aging in a single animal, such as flies or mice, or in different human tissues. However, a protein associated with aging in one species may not be relevant to the aging function in a different animal. This limitation had made it difficult to study the universal processes involved in aging.
Kim's work overturns a commonly held view that all animals, including humans, age like an abandoned home. Slowly but surely the windows break, the shingles fall off and floorboards rot, but there's no master plan for the decay.
That theory has left open questions about why tortoises and rockfish are still partying like 20-somethings at an age when humans are considered relics. At the other end of the spectrum, flies die off before young humans can even focus their eyes. Clearly, not all cells fall apart at the same rate.
"Aging isn't like the speed of light; it's not a constant," said Kim. Why animals and even people age at different rates prompted Kim to look deeper into the processes that control aging.
His new study suggests that the cell has a molecular homeowner that keeps up repairs until a predetermined time, when the owner picks up the welcome
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Contact: Amy Adams
amyadams@stanford.edu
650-723-3900
Stanford University Medical Center
20-Jul-2006