A new discovery shows the path to better anti-ageing treatment in future.
Researchers at the MDI Biological Laboratory, with collaboration with a group of scientists from the Buck Institute for Research on Ageing in Novato, California and Nanjing University in China have noticed some synergistic cellular pathways that can implement longevity in living beings. These pathways can ensure simplified lifespan.
To prove the fact, an experiment was conducted on the models of C.elegans, a nematode worm. The lifespan increase would be as good as living for almost 400 to 500 years.
The research draws on the discovery of two major pathways governing ageing in C. elegans, which is a popular model in ageing research because it shares many of its genes with humans and because it's short lifespan of only three to four weeks allows scientists to quickly assess the effects of genetic and environmental interventions to extend healthy lifespan.
Because these pathways are "conserved," meaning that they have been passed down to humans through evolution, they have been the subject of intensive research. A number of drugs that extend healthy lifespan by altering these pathways are now under development. The discovery of the synergistic effect opens the door to even more effective anti-ageing therapies.
The new research uses a double mutant in which the insulin signalling (IIS) and TOR pathways have been genetically altered. Because alteration of the IIS pathways yields a 100 per cent increase in lifespan and alteration of the TOR pathway yields a 30 per cent increase, the double mutant would be expected to live 130 per cent longer. But instead, its lifespan was amplified by 500 per cent.
"Despite the discovery in C. elegans of cellular pathways that govern ageing, it hasn't been clear how these pathways interact," said Hermann Haller, M.D., president of the MDI Biological Laboratory.
"By helping to characterize these interactions, our scientists are paving the way for much-needed therapies to increase healthy lifespan for a rapidly ageing population," he added.
The elucidation of the cellular mechanisms controlling the synergistic response is the subject of a recent paper in the online journal Cell Reports entitled "Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity." The authors include Jarod A. Rollins, Ph.D., and Aric N. Rogers, Ph.D., of the MDI Biological Laboratory.
"The synergistic extension is really wild," said Rollins, who is the lead author with Jianfeng Lan, Ph.D., of Nanjing University. "The effect isn't one plus one equals two, it's one plus one equals five. Our findings demonstrate that nothing in nature exists in a vacuum; in order to develop the most effective anti-ageing treatments we have to look at longevity networks rather than individual pathways."
The discovery of the synergistic interaction could lead to the use of combination therapies, each affecting a different pathway, to extend healthy human lifespan in the same way that combination therapies are used to treat cancer and HIV, Pankaj Kapahi, Ph.D., of the Buck Institute, has said. Kapahi is a corresponding author of the paper with Rogers and Di Chen, Ph.D., of Nanjing University.
The synergistic interaction may also explain why scientists have been unable to identify a single gene responsible for the ability of some people to live to extraordinary old ages free of major age-related diseases until shortly before their deaths.
The paper focuses on how longevity is regulated in the mitochondria, which are the organelles in the cell responsible for energy homeostasis. Over the last decade, accumulating evidence has suggested a causative link between mitochondrial non-regulation and ageing. Rollins' future research will focus on the further elucidation of the role of mitochondria in ageing, he concluded.
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