¶ … online scientific publication for current research on the role of the cell cycle in aging.
"Loss of Stem Cells Correlates With Premature
Aging In Animal Study." ScienceDaily 8 June 2007. 29 April 2009 http://www.sciencedaily.com/releases/2007/06/070606235257.htm
While dying and aging are accepted as inevitable facts of life, new research suggests that like so many diseases, aging (or at very least the rate at which we age) is encoded in our genes. Also, new research into what parts of the cell are involved in regeneration hold the promise for forestalling the seemingly inevitable symptoms of growing older. According to the ScienceDaily article "Loss of Stem Cells Correlates With Premature Aging In Animal Study," researchers at the Abramson Family Cancer Research Institute of the University of Pennsylvania have found that deleting a gene known as ATR from a mouse's genetic sequence can lead to premature aging and loss of stem cell reservoirs in the affected mice.
This gene, which is essential for normal cell regeneration allows the body to heal normally, in response to damaged DNA. Daily, the body breaks down and rebuilds itself. Our body's ability to regenerate slows down as we age and our reserves of stem cell reservoirs grows smaller, or in some cases loses their integrity through overly frequent division when our systems are particularly stressed. Until now, scientists were uncertain as to why this was the case, on a molecular level. The new model offered by this research could provide scientists with clues as to how to preserve stem cells and suppress or reduce the symptoms of aging and develop new ways to repair DNA damage due to cancer and other disorders in humans on a cellular level.
Aging may be described as a slow loss of stem cells, according to the researchers. The article stated: "To be able to renew itself, most tissues have a reservoir of specific adult stem cells. These stem cells don't divide as frequently as other cell types since they need to maintain the integrity of their DNA, and multiple divisions lead to natural breaks in DNA. But when these stem cells are needed, their progeny can rapidly divide and are able to replenish the tissue with new cells." Without such replenishment, the mice without the normal reserves of ATR had graying hair and hair loss, and osteoporosis, within three to four months. The "10 to 20% of cells that escaped ATR deletion were able to reconstitute tissues in the engineered mice, at least initially. However, it appears that in the long run, even these cells were insufficient to maintain tissue integrity." The ATR deletion speeded up the slow loss of stem cells that come with aging. Of course, the hope now is that researchers can find a way to add to the pool of cells for the mice in a way that can be useful for humans. Repairing the ATR that was deleted is the step in the research, and it is an open question as to whether this can forestall or even reverse aging.
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