To Defeat Frailty

To Defeat Frailty: "Viewpoints on aging - on therapies, what aging is, and how much can be done to stop it - continue to change for the better. From the San Franciso Chronicle: 'Researchers are finding that frailty may not be the inevitable result of aging but rather is a preventable and perhaps treatable condition. The muscle weakness, exhaustion, and weight loss typical of frailty were until recently considered just byproducts of diseases and the general loss of vitality during one's advanced years. Now scientists are studying the condition in its own right.' The article looks at very early first steps, both in opinions of aging and medical science. In the years ahead, we will be able to do far more to prevent aspects of age-related degeneration and thus extend healthy life span - but only if a foundation of widespread support and understanding for scientific longevity research is set down now.

View the Article Under Discussion: http://sfgate.com/cgi-bin/article.cgi?f=/c/a/2006/09/10/MNGRIL07L01.DTL
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/"

Studies find general mechanism of cellular aging

Studies find general mechanism of cellular aging: "Three separate studies confirm a gene that suppresses tumor cell growth also plays a key role in aging. Teams from the medical schools at the University of North Carolina at Chapel Hill, University of Michigan and Harvard University observed similar results in pancreatic islet cells and brain and blood stem cells."

A Mechanism of Cellular Aging

A Mechanism of Cellular Aging: "Via EurekAlert!, a biomechanism of cellular aging: 'Three separate studies confirm a gene that suppresses tumor cell growth also plays a key role in aging. The researchers found increasing concentration, or expression, of the gene p16INK4a in older cells; these aging cells worked poorly compared to young cells and remembered their 'age' even when transferred from old mice to young mice. ... The studies indicate that certain stem cells lose their ability to divide and replace themselves with age as the expression of p16INK4a increases ... even though old mice lacking p16INK4a show enhanced stem cell function, they do not live longer. This is because p16INK4a is an important cancer-suppressor gene, and mice lacking p16INK4a develop more cancers than old, normal mice ... p16INK4a loss was associated with an improvement in some but not all of the consequences of aging.' The age-old story: cancer or aging, pick one. Setting forth to repair the accumulation of damage seems like a better plan than tweaking the mechanism for greater performance at this point.

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