Researchers at the Salk Institute for Biological Studies have found that slowing the engines of mitochondria, the tiny cellular factories, could extend your life span.
Andrew Dillin and his colleagues demonstrated their experiment on the roundworm Ceanorhabditis elegans to show that perturbing mitochondrial function in subsets of worm cells sent global signals governing longevity of the entire organism.
"In this study we show how signals sent from distressed mitochondria are communicated to distant tissues to promote survival and enhance longevity," said Dillin.
The identity of the signal sent from mitochondrially - distressed cells - a hypothetical factor called a 'mitokine' - remains unknown.
"Imagine if we could perturb mitochondria in the liver, and make them send a mitokine to degenerating neurons. Instead of trying to get a drug into the brain, we could exploit the body's ability to send out a natural rescue signal," said Dillin.
The team observed the relationships between mitochondria, energy generation and longevity and found that living long does not necessarily require prospering at the subcellular level.
"Many genes were related to mitochondrial function. If you disabled them, worms lived longer, although their respiration or metabolism was reduced. We wondered whether this is why animals lived longer," he said.
However, there's a catch that was discovered in the current study.
"It was like you could manipulate mitochondria in a 30-year-old human and get an extra 15 years, while in an 80-year-old, you might only gain two or three years," he said.
The study appears in the Jan. 7, 2011, issue of Cell.