Biologists beat back death in fruit flies. Humans next?
Researchers at the University of California, Los Angeles (UCLA) have figured out a way to extend the life of female fruit flies by 20 percent by manipulating what the school has called a "cellular time machine." The biologists who carried out the work are hopeful that their findings will have implications for human aging and help fight off age-related diseases like Alzheimer's and Parkinson's.
The researchers focused on mitochondria, tiny structures that act a bit like digestive organs inside our cells. These "cellular power plants" take the chemicals and oxygen in our systems provided through food and respiration, and convert them into a molecule known as ATP, which the cell can then use as food. When mitochondria age however, they can become damaged and build up in the body, creating a toxic environment conducive to disease formation.
In the research, UCLA biologists studied the mitochondria in fruit flies and figured out that as the insects reach middle age – which, for a fruit fly, is about one month old – their mitochondria change shape, making it tough for their cells to clear them out when the organelles are no longer functioning properly.
"We think the fact that the mitochondria become larger and elongated impairs the cell's ability to clear the damaged mitochondria," said David Walker, a UCLA professor of integrative biology and physiology, and the study's senior author. "And our research suggests dysfunctional mitochondria accumulate with age, rather than being discarded."
So the scientists gave the flies a hand by increasing a protein called Drp1 for one week when they reached 30 days of age. The result was that the damaged mitochondria was broken up into smaller pieces that the flies were able to expel from their cells. This not only led female flies to live about 20 percent longer and male flies to live about 12 percent longer than their typical two-month lifespans, but the researchers also found that the flies had increased energy levels and endurance.
What's more, the boost in Drp1 also held off a condition in which the flies get leaky intestines about a week before they die. The condition is not only a precursor to death in fruit flies but it has also been implicated in the death of monkeys, worms and mice.
"It's like we took middle-aged muscle tissue and rejuvenated it to youthful muscle," said Walker. "We actually delayed age-related health decline. And seven days of intervention was sufficient to prolong their lives and enhance their health."
The biologists also further experimented with a protein called Mfn, which keeps mitochondria from clumping together and getting too big for cells to deal with. When they turned its production off in the flies, they saw similar benefits in terms of health and life extension.
"You can either break up the mitochondria with Drp1 or prevent them from fusing by inactivating Mfn," said Anil Rana, a UCLA project scientist and the study's lead author. "Both have the same effect: making the mitochondria smaller and extending lifespan."
The team hopes that it may eventually be possible to create a drug that would work in the same way as the proteins to not only extend and improve the lives of humans, but to help stave off age-related diseases. Walker points to the fact that the treatment worked so fast as a major plus, considering that it could lessen the negative effects often associated with the long-term use of pharmaceuticals.
The findings have been reported in the journal Nature Communications.