The findings will help researchers better understand the molecular mechanisms that drive ageing and risk for age-associated degenerative diseases.
‘Small amounts of stress may be desired, beneficial, and even healthy. Signals from mildly stressed mitochondria prevent the failure of protein-folding quality control machinery that comes with age.’
"Our findings offer us a strategy for looking at ageing in humans and how we might prevent or stabilise against cell decline as we age," said Richard I. Morimoto, Professor at the Northwestern University.
"Our goal is not trying to find ways to make people live longer but rather to increase health at the cellular and molecular levels, so that a person's span of good health matches their lifespan," Morimoto added.
For the study, published in the journal Cell Reports, the team screened a transparent roundworm C. elegans' approximately 22,000 genes.
The researchers found that signals from mildly stressed mitochondria -- the cellular source of energy -- prevent the failure of protein-folding quality control (proteostasis) machinery that comes with age.
This, in turn, suppresses the accumulation of damaged proteins that can occur in degenerative diseases, such as Alzheimer's, Huntington's and Parkinson's diseases and amyotrophic lateral sclerosis (ALS).
"People have always known that prolonged mitochondrial stress can be deleterious. But we discovered that when you stress mitochondria just a little, the mitochondrial stress signal is actually interpreted by the cell and animal as a survival strategy," Morimoto said.
"It makes the animals completely stress-resistant and doubles their lifespan. It's like magic," he added.
C.elegans has a biochemical environment and cellular properties similar to that of humans. The findings in the transparent roundworm may have implications for humans and quality of life.