Finding might one day lead to extended life spans
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.
"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.
"Mice lacking SIRT6 seem to hit some kind of a wall at around 4 weeks of age when their blood sugar drops to a level barely compatible with life," Dr. Katrin Chua, assistant professor of endocrinology, gerontology and metabolism at Stanford, said in the news release. "Reducing NF-kB activity somehow allows the mice to get over this critical period and to live much longer."
Trying to figure out how NF-kB knows the timing and extent of its role in aging and how SIRT6 might affect this is the next step for the researchers.
"It's a very provocative question," Chang said. "We've tied together two previously separate pathways in aging. Now we'd like to better understand what regulates that pathway."
The U.S. Centers for Disease Control and Prevention has more about healthy aging.
-- Kevin McKeever
SOURCE: Stanford University, news release, Jan. 8, 2009
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