Age may not be rust after all. Specific genetic instructions drive aging in worms, report researchers at the Stanford University School of Medicine. Their discovery contradicts the prevailing theory that aging is a buildup of tissue damage akin to rust, and implies science might eventually halt or even reverse the ravages of age.
“We were really surprised,” said Stuart Kim, PhD, professor of developmental biology and of genetics, who is the senior author of the research.
Kim’s lab examined the regulation of aging in C. elegans, a millimeter-long nematode worm whose simple body and small number of genes make it a useful tool for biologists. The worms age rapidly: their maximum life span is about two weeks.
Comparing young worms to old worms, Kim’s team discovered age-related shifts in levels of three transcription factors, the molecular switches that turn genes on and off. These shifts trigger genetic pathways that transform young worms into geezers. The findings will appear in the July 24 issue of the journal Cell.
The question of what causes aging has spawned competing schools of thought. One side says inborn genetic programs make organisms grow old. This theory has had trouble gaining traction because it implies that aging evolved, that natural selection pushed older organisms down a path of deterioration. However, natural selection works by favoring genes that help organisms produce lots of offspring. After reproduction ends, genes are beyond natural selection’s reach, so scientists argued that aging couldn’t be genetically programmed.
The alternate theory holds that aging is an inevitable consequence of accumulated wear and tear: Toxins, free-radical molecules, DNA-damaging radiation, disease and stress ravage the body to the point it can’t rebound. So far, this theory has dominated aging research.
But the Stanford team’s findings told a different story. “Our data just didn’t fit the current model of damage accumulation, and so we had to consider the alternative model of developmental drift,” Kim said.