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Researchers at the Stanford University School of Medicine have reversed the effects of aging on the skin of mice, at least for a short period, by blocking the action of a single critical protein.
The work could one day be useful in helping older people heal from an injury as quickly as they did when they were younger, said senior author Howard Chang, MD, PhD, assistant professor of dermatology. However, Chang and his colleagues warned their finding will likely be useful in short-term therapies in older people but not as a potential fountain of youth.
The work backs up the theory that aging is the result of specific genetic changes rather than accumulated wear and tear, Chang said. What’s more, those genetic changes can be reversed even late in life.
“The implication is that the aging process is plastic and potentially amenable to intervention,” Chang said. The results will be published in the Dec. 15 issue of the journal Genes and Development.
The work came about thanks to existing data from experiments using microarrays, which detect the activity of all genes in a cell. In past experiments, researchers have found a large number of diverse genes that become either more active or less active in older people.
Chang and graduate student Adam Adler, the study’s first author, searched through this existing data to see if those age-related genes had anything in common. It turned out that their activity gets dialed up or down with the help of the protein called NF-kappa-B.
Chang said people had long known that NF-kappa-B winds its way into a cell’s nucleus to control which genes were active. What they didn’t know is that many of those genes regulated by the protein have a role in aging.