LONGEVITY GENE IN FRUIT FLIES HINTS AT COMING GENETIC DISCOVERIES TO SLOW AGING
Written By: Jason Dorrier
In the last few centuries, medical advances have greatly lengthened lifespans. Among other causes, a central driver has been improved care at the beginning of life, when declining infant mortality rates have boosted average life expectancy at birth.
Now, as more people live into their eighties, nineties, and beyond, researchers are focusing on the end of life. And with the increasing incidence of age-related diseases, like Alzheimer’s and cancer, it’s not just prolonging life, but prolonging health too.
Some believe the answer to a long, healthy life lies hidden in our genes.
In a recent study, researchers at the University of California Los Angeles (UCLA), say that activating a gene, AMPK, in fruit flies’ intestines was found to add 30% to their average lifespans—up to eight weeks from the typical six weeks.
Beyond simply boosting lifespans, the flies stayed healthier too.
The research found that activating the gene increased the rate of a cellular processcalled autophagy, in which cells break down damaged cellular components and proteins that can negatively affect cell health. This cellular junk tends to accumulate as we age.
In addition, activating the gene in one organ appeared to have wider ranging effects.
UCLA’s David Walker.
“We have shown that when we activate the gene in the intestine or the nervous system, we see the aging process is slowed beyond the organ system in which the gene is activated,” said David Walker, UCLA associate professor of integrative biology and physiology and senior author of the research.
The fact that turning on the gene in one place slows aging elsewhere may simplify future treatments for age-related disease in humans—the researchers’ long-term goal. This is because developing therapies for some organs, like the intestines, may prove to be technically much simpler than developing therapies for others, like the brain.
Fruit fly studies are a great place to start for genetic research. Scientists have intimate knowledge of the insect’s genome and have learned to activate and deactivate individual genes. This particular study looked at over 100,000 genes.
However, there is, of course, a difference between fruit flies and humans. And although extending human longevity is the goal, scientists are still years from achieving it.
Longevity studies, in general, have a fraught history wherein promising new discoveries get an avalanche of press only to fall from favor a few years later. In this case, additional research, especially in human populations, is necessary.
Beyond potential therapeutic uses, however, its finding that increased autophagy can lengthen life is intriguing on its own. Aubrey de Grey’s SENS Research Foundation, an organization focused on the study of human longevity, outlines seven categories of cellular damage that, added up over a lifetime, result in aging and age-related disease.
Two of the seven categories target the accumulation of junk protein in and around cells.
Alzheimer’s disease is perhaps the best known example of such accumulation. The brains of Alzheimer’s patients are a mess of misfolded proteins called plaques and tangles. It’s thought these malfunctioning proteins cause parts of the brain to die off.
A number of big drug trials targeting brain plaques have failed in recent years, confounding pharmaceutical firms and researchers alike. But some have suggested a major shortcoming is diagnosis—that is, by the time behavioral symptoms show up, significant fractions of the brain have already died and damage can’t be reversed.
Flipping a genetic switch early on, however, would be a bit like ordering the body’s natural cellular maid service more regularly—or like doing the dishes as you use them as opposed to waiting days to tackle teetering stacks of crusty bowls and plates.
Further study will hopefully learn more precisely how such genetic switches work, what they control, and perhaps find more of them. Longevity likely involves the interplay of a number of genes. This is why the plummeting cost of genomic sequencing is so exciting. Mass studies are just now getting underway.
Genomic sequencing pioneer, Dr. Craig Venter, founded Human Longevity Inc. earlier this year and seeded it with two cutting-edge genomic sequencers. These Illumina sequencers can transcribe thousands of genomes a year at $1,000 per genome—a simply massive improvement.
It took years and hundreds of millions of dollars to sequence a single human genome a decade ago—Human Longevity Inc. aims to sequence 40,000 human genomes a year.
For Venter’s firm and other research organizations, these advances in genomic sequencing, paired with better and more automated data analysis software, may accelerate the discovery of genes linked to longevity and age-related disease. Perhaps we’ll soon know the human genome as intimately as we know the fruit fly’s.
Alone, it’s probably wise not to read too much into the recent UCLA study for now. More broadly, however, the study’s findings offer a tantalizing glimpse into the potential power of coming genetic discoveries. That is, it’s likely only the beginning of the story.
Image Credit: Shutterstock.com; UCLA
This entry was posted in Genetics, Longevity And Health and tagged age-related disease, Aubrey De Grey, Craig Venter, David Walker, genomics, Human Longevity Inc., illumina, Illumina HiSeq X Ten,longevity, SENS Foundation, UCLA.