Biologists from the University of California Los Angeles (UCLA) have developed an intervention that serves as a cellular time machine – the clock returns to the key component of aging
In a study of middle-aged fruit flies, scientists have significantly improved animal health and significantly slowed down their aging at the same time. They believe that the technique could ultimately lead to postponement of Parkisnon's disease, Alzheimer's disease, cancer, stroke, cardiovascular disease and other age-related diseases.
The approach focuses on mitochondria, small energy generators within cells that control cell growth and determine if they will live or die. Mitochondria is often damaged with age, and people are aging, so damaged mitochondria accumulate in the brain, muscles and other organs. When cells that can not remove damaged mitochondria, these mitochondria can become toxic and contribute to a wide range of age-related diseases, said David Walker, professor of Integrative Biology and Physiology at UCLA and senior author of the study.
In a new study, Walker and his colleagues found that mitochondria in fruit flies that reached middle ages – one month within their two-month life span – changed from their original small round shape
"We think the fact that mitochondria become larger and longer distorts the cell's ability to purify damaged mitochondria," Walker said. "Our research suggests that dysfunctional mitochondria accumulate with the years instead of being rejected."
The study, published a couple of days ago in Nature Communications reports that UCLA scientists removed damaged mitochondria by breaking larger mitochondria into smaller parts – and when they did, flies became more energetic and more durable. In observations after treatment it was noted that female fruit flies lived 20 percent longer than their normal life, while males lived on average 12 percent longer.
Scientists emphasized the importance of protein Drp1 in aging. At least in flies and mice, the levels of protein Drp1 decrease with age.
In order to break up the mitochondria flies, Anil Rana, a UCLA scientist and study leader increased their protein levels in Drp1. This has enabled flies to reject minor, damaged mitochondria and remain only healthy mitochondria. Systematic increase in Drp1 levels lasted for a week, and began when flies were 30 days old.
At the same time, Rana showed that gene Atg1 in flies also plays an important role in turning the clock cell aging. This was done by "extinction" of the gene, which caused the flies to fail to remove the damaged mitochondria. This has been shown by the fact that the gene Atg1 is needed to restore anti-aging effects within this process: while Drp1 breaks down the increased mitochondria, the Atg1 gene is needed to remove the injured.
"It's as if we took middle-aged muscle tissue and rejuvenated it to the young muscle," said Walker, a member of UCLA's Institute of Molecular Biology. "We actually postponed the loss of age-related health. Seven days of intervention was enough to extend their lives and improve their health. "
One specific health problem that treatment addresses is bowel leakage that Walker's team in previous research has found to commonly occur one week before the death of a fruit fever. Subsequent research in other laboratories has revealed that increased bowel permeability is a sign of aging in worms, mice and monkeys. In a study conducted at UCLA, the condition was postponed after the flies had received more Drp1
Fruit flies are often used in aging research because their short life span allows scientists to monitor the effects of certain treatments within a short period of time, and many aging characteristics at the cellular level are similar to those in humans. In addition, scientists have identified all the genes of fruit fever and know how to turn on or off some of them.
Walker hopes that a technique like this developed by his team of fruit flies could one day help people compare aging and postponement of age-related illness. He said that the fact that the new approach was effective even after a short time has great importance because long-term use of almost any drug can have harmful consequences for humans.
Walker said it was one of the long-term goals of his research to develop drugs that will mimic the effects of the Drp1 protein, with the aim of prolonging the lives of humans but also what he calls "the age of health" – the number of healthy years in life.
In the second part of the experiment, which was also carried out in middle-aged fruit flies, scientists have blocked the Mfn protein that allows mitochondria to bind into larger pieces. This also lengthened the life of flies and improved their health.
"It can or break mitochondria with protein Drp1 or can be prevented from binding to activation of protein Mfn," said Rana. "Both have the same effect: reducing mitochondrial size and prolonging life expectancy."
The function of Drp1 protein in animals was discovered by Alexander van der Bliek, a professor of biological chemistry at UCLA in the early 2000s, Science Daily