Scientists extend the lifespan of a roundworm that is genetically comparable to people by 500 percent
Could WORMS keep secret from anti-aging? Scientists extend the life of a roundworm that is FIVE times genetically comparable to humans
- American and Chinese scientists used mutations to adjust the lifespan of a roundworm
- C. elegans normally lives for three weeks but had extended its lifespan fivefold
- The roundworm shares genetic traits with people because of a common ancestor
- The study can help in the development of drug combinations for people who delay aging
Scientists have succeeded in extending the lifespan of a worm by 500 percent in a surprising discovery that could hold the secret of anti-aging in humans.
Caenorhabditis elegans, a roundworm that shares genetic traits with humans, normally lives for about three to four weeks.
By adjusting a few cellular routes, the American and Chinese research team were able to develop a worm that lived for more than 14 weeks – a five-fold increase.
This increase in lifespan would be the equivalent of a person who lives around 400 to 500 years.
The discovery could lead to comparable combination therapies for people who prolong the aging process, just as combination therapies are currently used to treat cancer and HIV.
Caenorhabditis elegans is a free-living, transparent nematode or roundworm, approximately 1 mm long
WHY SCIENTISTS USE C.ELEGANS TO STUDY HUMAN DISEASES?
C. elegans is a small soil worm or nematode.
It shares a common ancestor with people – known as the urbilaterian ancestor.
This ancestor, who lived 500 – 600 million years ago, is the family member of all bilaterally symmetrical, multicellular organisms, including mammals.
Most genes involved in human development and disease were present in the urbilaterian ancestor.
Evolution is a process whereby existing genetic mechanisms are retained, but modified slightly, to result in different species.
As a result, C. elegans have neurons, skin, intestines, muscles, and other tissues that resemble humans in form and function.
Both the ISS and TOR path in the roundworm study are ‘preserved’, which means that they have been passed on to humans through evolution.
Developmental mechanisms in C. elegans help to understand the fundamental, core mechanisms that also work with people.
Source: the University of Kansas
C. elegans is a non-parasitic type of worm Nematoda phylum, approximately 0.03 inch long.
The species is used by scientists in aging research because it actually shares many of its genes with humans because both species share a common ancestor.
This agreement allows scientists to assess the effects of genetic and environmental interventions in the worms to investigate how the lifespan can be extended.
American and Chinese scientists used two major cellular pathways – insulin signaling (IIS) – which connects nutrient levels with metabolism, growth, and lifespan – and TOR pathways – a nutrient-sensitive, central cell growth and aging controller.
The team introduced a “double mutant” in which both routes were genetically modified.
Previous research has shown that changing the IIS routes results in a 100 percent longer lifespan, while changing the TOR route results in a 30 percent longer lifespan.
For this reason, the team was surprised to discover a five-fold total increase in lifespan and not a 130 percent increase as predicted.
“The synergistic extension is really wild,” Dr. said. Jarod Rollins, assistant professor at the MDI lab and lead author of the study.
“The effect is not one plus one is two; it’s one plus one is five.
“Our findings show that nothing in nature exists in a vacuum; To develop the most effective anti-aging treatments, we need to look at networks with a long lifespan instead of individual routes. ”
C. elegans has been used extensively as a model organism to understand biological phenomena such as aging
A number of drugs that extend the TOR and IIS routes are under development, but it may take a while for the technique to be equally effective in humans.
“Tweak activity of similar genes in people with drugs or other therapeutics, while unlikely to cause a 500 percent lifetime extension, can cause a similar kind of synergistic effect when both gene pathways are targeted at the same time,” Dr. Rollins told MailOnline .
“It is unlikely that the same changes in humans as in our paper cause a five-fold increase in life span because we are more complex than the nematode – we have adaptive immunity, cardiovascular systems and complex brains that do not have these worms.
“It is likely that we will gain a deeper understanding of how all these systems interact before we can have similar extensions, people who promote life with the risk of side effects.”
A trial with treatments for human aging is a project called Targeting Metformin with Aging (TAME), according to Dr. Rollins, that will look at the effect of a commonly used diabetes drug to slow the progression of age-related diseases.
Further research will now work to clarify the role of mitochondria – the “powerhouse” of the cell responsible for energy homeostasis – in aging.
The detailed study of the team on how longevity is regulated in the mitochondria of the cell is published in Cell Reports.