Delving deep into the molecular subtleties of a strain of mice engineered to age rapidly, scientists have found that an accumulation of genetic mutations prompts a cascade of programmed cell death that seems to underpin the aging process.
Writing today (July 15, 2005) in the journal Science, a team of scientists led by University of Wisconsin-Madison geneticist Tomas A. Prolla describes a series of experiments in mutant and normal mice that peel away some of the root secrets of mammalian aging.
Growing old, according to the new study, occurs, in part, as mutations build up in the DNA of energy-generating mitochondria, triggering the death of critical cells that lead to such things as hair and weight loss, hearing and vision impairment, loss of muscle mass, weakened bones and fewer circulating red blood cells. Mitochondria are structures within cells that provide energy for cells to move, divide, contract and secrete products vital for the health of organisms. "We think that the key to what is happening in aging is that as (genetic) mutations or DNA damage accumulates, critical cells die," says Prolla. "These experiments favor a major role for programmed cell death in aging."
Tomas A. Prolla | EurekAlert!
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