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From Botox and plastic surgery to red sports cars and Rogaine, it seems everybody wants to be younger.

And while science has not uncovered a method to prevent aging altogether, stem cell scientists at Penn recently uncovered new information that may be useful in slowing down the aging process.

According to a June 6 press release, researchers at the University's Abramson Family Cancer Research Institute found that deleting a gene called ATR in adult mice can lead to premature aging including hair loss and osteoporosis.

The gene ATR is instrumental in repairing damaged DNA in the body, which in turn decreases the risk of certain forms of cancer and other diseases as well as suppresses aging.

This discovery is important because it helps untangle the many mysteries of the aging process in both mice and humans, as well as shed light on the relationship between stem cells, DNA repair and aging.

According to the press release, adult stem cells are used to repair and replenish damaged tissue as the body ages.

However, the more these stem cells divide and are utilized, the more likely their DNA is to become damaged in some way. The gene ATR, which has an important role in repairing damaged DNA, ensures that these stem cells reach their full potential in replenishing damaged tissue and thus stave off aging as long as possible.

So, when the ATR in adult mice was deleted during the course of the research, these mice were unable to renew damaged tissue and thus began to age rapidly.

To Eric Brown, the Cancer Biology professor who headed the project, the research has many far-reaching implications. Now that he and his team know that DNA repair and stem cells are an instrumental part of the aging process they can try to find a way to slow that process down.

"If we can identify the main cause of stem cell loss and slow down stem cell loss, then we could prevent certain age-related diseases and slow particular aspects of the aging process," he said.

Amma Asare, a 2006 College graduate and a research technician on the project, echoed Brown in this regard.

"Our research looked at the mechanisms of aging; the next step would be to look at therapies to slow the process down," she said.

And according to the press release, Brown, Asare and their team, including first author and post-doctoral researcher Yaroslava Ruzankina, "are currently using the mouse model to discover compounds that preserve stem cells and may, consequentially, suppress aging."

Brown noted that the aging process that his team discovered in mice is almost certainly similar in humans.

"Yes, similar processes might govern aspects of human aging, although further research will be necessary to verify that," he said.

Thus, what is good for the mice is probably good for humans.

And while Brown and his team are busy trying to make lives a little longer, Penn is a few weeks away from opening a brand new stem cell institute that would span multiple schools at the University, said Jonathan Epstein, chairman of Penn's Cell and Developmental Biology Department.

"Penn is in the negotiation stages for a stem cell institute," he said. "It's very important that we take a lead in this area."

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