- Researchers identify cellular pathways for increasing the lifespan of C.elegans by 500%.
- The incredible gain of C. elegans lifespan would be equivalent to a human living for approximately 500 years.
Highly conserved insulin-like signaling (IIS) and target of rapamycin (TOR) play a crucial role in aging across species. To modulate aging, scientists have been examining the interaction between these pathways for years.
Now, a research team at the MDI Biological Laboratory, Nanjing University, and Buck Institute for Research on Aging has successfully identified cellular pathways responsible for increasing the lifespan of C.elegans by 500%.
C. elegans is a transparent, free-living nematode worm, about 1 millimeter in length. It’s a non-infectious, non-hazardous, and non-parasitic organism that lives in temperate soil environments.
Since C. elegans have neurons, gut, muscles, skin and other tissues that are very similar in genetics and functions to those of humans, they are widely studied for various research purposes.
Modifying Pathways To Extend Healthy Lifespan
In this study, the short lifespan (of only 3-4 weeks) of C.elegans allowed researchers to analyze the effects of genetic and environmental interventions to increase the human lifespan.
A few drugs that modify these pathways (to extend healthy lifespan) are now being developed. In summary, the findings open new avenues to even more advanced anti-aging treatments.
Both pathways (IIS and TOR) have been genetically modified using a double mutant. Modification of the ISS pathways results in a 100% increase in lifespan and modification of the TOR pathways leads to a 30% increase. This means the double mutant should live 130% longer. But surprisingly, its lifespan was extended by 500%.
The 500% increase of C. elegans lifespan would be equivalent to a human living for approximately 500 years.
In addition to discovering age-governing cellular pathways in C.elegans, researchers characterize the interactions between these pathways. This paves the way for effective therapies required to amplify the healthy lifespan of a rapidly aging population.
Rather than looking at individual pathways, researchers focused on longevity networks. The synergistic interaction discovered in this study could enable combination therapies (each influencing different pathways) to increase healthy lifespan, just as existing combination therapies are used to treat HIV and cancer.
This synergistic interaction could also uncover why scientists haven’t been to spot a single gene that allows some people to live to extraordinary old ages free of severe age-associated disorders.
The study also describes how longevity is controlled in the mitochondria, a membrane-bound-organelle found in most eukaryotic organisms.
The evidence accumulated over the past 10 years has indicated a causative link between aging and mitochondrial dysregulation. In the future, researchers will explore the role of mitochondria in aging.