Biologists slow aging in flies
Image: Fruit flies' mitochondria (in green) over time and rejuvenated (bottom right) [Nature Communications/Anil Rana]
US-based biologists have developed a 'cellular time machine' that works on flies and could one day be used to slow aging and extend the lifespan of humans.
Stunning images reveal how the flies' mitochondria - the power generators within cells that control growth - return to a more youthful state after increasing levels of a protein called Drp1.
The method enables damaged mitochondria to be more effectively removed from organs, in effect, turning back the clock on a key component of aging.
Professor David Walker from Integrative Biology and Physiology at the University of California Los Angeles, and colleagues, believe the technique could help to delay the onset of Parkinson's disease, Alzheimer's disease, cancer and other age-related diseases in humans.
As Walker highlights, mitochondria often become damaged with age, and as people grow older, those damaged mitochondria tend to accumulate in the brain, muscles and other organs.
When cells can't eliminate the damaged mitochondria, these organelles can become toxic and contribute to a wide range of age-related diseases.
In their research, Walker and his colleagues found that as a fruit fly reaches middle age - about one month into their two-month lifespan - its mitochondria change from an original small, round shape.
"We think the fact that the mitochondria become larger and elongated impairs the cell's ability to clear the damaged mitochondria," explains Walker. "And our research suggests dysfunctional mitochondria accumulate with age, rather than being discarded."
To combat this, the researchers removed the damaged mitochondria by breaking up enlarged mitochondria into smaller pieces, and watched as the flies became more energetic and showed greater endurance.
As Walker points out, to break apart the mitochondria, he and colleagues increased the levels of so-called dynamin-related protein 1 within the flies.
Levels of Drp1 decline as flies age, but the protein boost enabled the flies to discard the smaller, damaged mitochondria, leaving only healthy mitochondria.
Following treatment, female flies lived 20 percent longer than their typical lifespan, while males lived 12 percent longer, on average.
At essentially the same time, the researchers also demonstrated that the flies' Atg1 gene also plays an essential role in turning back the clock on cellular aging.
'Turning off' the gene, rendered the flies' cells unable to eliminate the damaged mitochondria.
According to the researchers, this proved that Atg1 is essential to their procedure's anti-aging effects: while Drp1 breaks up enlarged mitochondria, the Atg1 gene is needed to dispose of the damaged organelles.
Fruit flies' mitochondria (in green) at 10 days (top left), 28 days (top right) and 37 days old (both bottom images). At bottom right, the mitochondria have returned to a more youthful state after UCLA biologists increased the fly's level of a protein called Drp1. [Nature Communications/Anil Rana]
"It's like we took middle-aged muscle tissue and rejuvenated it to youthful muscle," highlights Walker. "We actually delayed age-related health decline. And seven days of intervention was sufficient to prolong [fly] lives and enhance health."
Walker hopes that a technique similar to the one his team developed for fruit files could eventually help humans by slowing aging and delaying aging-related diseases.
He reckons the fact that the new approach was effective even after a short time is especially significant because long-term use of nearly any drug can have harmful side effects in humans.
Research is published in Nature Communications.