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posted by janrinok on Saturday January 11 2020, @09:25AM   Printer-friendly
from the "who-wants-to-live-forever?" dept.

Biologists identify pathways that extend lifespan by 500%:

Scientists at the MDI Biological Laboratory, in collaboration with scientists from the Buck Institute for Research on Aging in Novato, Calif., and Nanjing University in China, have identified synergistic cellular pathways for longevity that amplify lifespan fivefold in C. elegans, a nematode worm used as a model in aging research.

The increase in lifespan would be the equivalent of a human living for 400 or 500 years, according to one of the scientists.

The research draws on the discovery of two major pathways governing aging in C. elegans, which is a popular model in aging research because it shares many of its genes with humans and because its 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-aging therapies.

The new research uses a double mutant in which the insulin signaling (IIS) and TOR pathways have been genetically altered. Because alteration of the IIS pathways yields a 100 percent increase in lifespan and alteration of the TOR pathway yields a 30 percent increase, the double mutant would be expected to live 130 percent longer. But instead, its lifespan was amplified by 500 percent.

"Despite the discovery in C. elegans of cellular pathways that govern aging, 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 aging population."

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 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 dysregulation and aging. Rollins' future research will focus on the further elucidation of the role of mitochondria in aging, he said.

More information:

Jianfeng Lan et al. Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity, Cell Reports (2019). DOI: 10.1016/j.celrep.2019.06.078

Journal information: Cell Reports


Original Submission

 
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  • (Score: 2) by HiThere on Saturday January 11 2020, @10:07PM

    by HiThere (866) Subscriber Badge on Saturday January 11 2020, @10:07PM (#942319) Journal

    We haven't studied the naked mole rat anything like long enough to say "they never naturally die".

    As for humans, one form of arthritis is caused by the body's self-repair not being perfect. I recently had an xray to check on something and was told I'd got extensive bone spurs at every joint of my spine, but that the only treatment was to cut me open and saw the spurs off, being careful to avoid sawing off the nerve trunks that were right next to them. My podiatrist said something similar, though less extreme, about my feet. And I'd barely noticed a problem yet.

    So don't expect your body's "self-repair" systems to work forever...at least not as what you think of as "self-repair". After all, the things doing it don't have a blueprint that they look at to see what the body should look like, they have a recipe on what to do in which chemical environment. And it didn't evolve expecting to survive forever. It might be possible to design a genetic code that would work (in principle, this is quite far beyond the state of the art), but the first thing to be improved would probably be the fidelity with which genes are copied. I think our current system is a bit more complex than the current repair mechanisms can hold stable. (Thus some forms of cancer. I'm excluding environmental insults from this problem.)

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