Activating a specific gene makes fruit flies live 30% longer
Model of an entire Drosophila head, with different sub-structures of the brain and nervous system colour coded.

A team of biologists has shown that activating a gene called AMPK in the fruit fly Drosophila melanogaster can add two weeks to their usual six-week lifespan.

And the fruit flies didn’t just live longer, their brains aged more slowly and they stayed healthier for longer as well.

AMPK is a gene that helps regulate energy in cells - when cellular energy levels are low, it gets activated. It’s also found in humans in low levels, which led the researchers to believe that understanding its pathway could help us work out how to delay our own ageing process.

As journalist Liat Clark explains for Wired magazine, the team are driven by the idea that by repairing the molecular damage that occurs as cells degrade, we can help to avoid diseases associated with ageing.

"Instead of studying the diseases of ageing - Parkinson's disease, Alzheimer's disease, cancer, stroke, cardiovascular disease, diabetes - one by one, we believe it may be possible to intervene in the ageing process and delay the onset of many of these diseases," David W Walker, a molecular biologist whose lab conducted the research at the University of California, Los Angeles (UCLA), said in a press release.

A key part of this cellular ageing process is a build up of “molecular garbage” - this is molecular waste that is usually cleared out through a process known as autophagy. But as we age, autophagy can slow down and molecular garbage and protein can build up, something that has already been linked to neurodegenerative diseases such as Alzheimer’s and Parkinson’s. 

Scientists have previously shown that AMPK  was known to activate authopahgy, but scientists weren’t sure of how this process occurred.

The research, led by Matthew Ulgherait from UCLA, involved stimulating AMPK in more than 100,000 fruit flies, and that activating AMPK in the intestine could increase levels of autophagy around the body - even in the brain. This is an important discovery, because in humans it would be much easier to trigger a similar process via the intestine rather than neurally.

“Matt moved beyond correlation and established causality,” Walker said in a press release. “He showed that the activation of autophagy was both necessary to see the anti-aging effects and sufficient; that he could bypass AMPK and directly target autophagy.” The research is published in Cell Reports.

Obviously this cellular pathway now needs to be tested in humans, but it’s a very promising first step towards better understanding the way our cells age - and potentially working out how to slow that natural process down.

Source: Wired, UCLA