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THURSDAY, Jan. 8 (HealthDay News) -- Stanford University researchers have linked two previously thought-to-be-separate pathways tied to aging, at least in mice, leading to more thought that physically getting older is an orderly and deliberate genetic occurrence.
Short-circuiting that process might one day allow scientists to extend life and delay aging, the researchers said.
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"There is a genetic process that has to be on, and enforced, in order for aging to happen," Dr. Howard Chang, associate professor of dermatology at the university's medical school, said in a news release issued by Stanford. "It's possible that those rare individuals who live beyond 100 years have a less-efficient version of this master pathway, just as children with progeria -- a genetic aging disease -- may have components of this pathway that are more active."
The findings, published in the Jan. 9 issue of Cell, link pathways involving the SIRT6 and NF-kappa B, or NF-kB, protein molecules. SIRT6, part of the sirtuin family of proteins, regulates life span in some simple organisms, and NF-kB regulates production of certain genes involved in aging. It has previously been found that blocking NF-kB activity in skin cells of elderly mice makes the cells look and act like younger cells.
The research team found that SIRT6 links up to an NF-kB subunit, possibly causing changes in humans and mice that make it harder for NF-kB to do its job.
"It seems that an important job of SIRT6 is to restrain NF-kB and limit the expression of genes associated with aging," Chang said.
But in genetically altered mice without the SIRT6 protein, the number of NF-kB-dependent genes involved in immune response, cell signaling and metabolism grows to a level that previous studies had shown could cause a fatal aging-like condition for mice less than 4 weeks old, the researchers said.
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-- Kevin McKeever
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