I've been following Valter Longo's work on fasting as a way to reduce
chemotherapy side effects while improving its effectiveness. His work
in that area was an outgrowth of his longevity research, including the
effects to calorie restriction.
---------- Forwarded message ----------
From: Eugen Leitl <
eu...@leitl.org>
Date: Mon, Jan 28, 2013 at 4:48 PM
Subject: [tt] Geneticists Discover a Way to Extend Lifespans to 800 Years
To:
t...@postbiota.org,
bio...@postbiota.org
http://io9.com/345728/geneticists-discover-a-way-to-extend-lifespans-to-800-%20years
Geneticists Discover a Way to Extend Lifespans to 800 Years
There is now a way to extend the lifespan of organisms so that humans could
conceivably live to be 800 years old. In an amazing development, scientists
at the University of Southern California have announced that they've extended
the lifespan of yeast bacteria tenfold — and the recipe they used to do it
might easily translate into humans. It involves tinkering with two genes, and
cutting down your calorie intake. Tests have already started on people in
Ecuador.
According to an announcement from PLoS Genetics:
Researchers have created baker's yeast capable of living to 800 in yeast
years without apparent side effects. The basic but important discovery,
achieved through a combination of dietary and genetic changes, brings
scientists closer to controlling the survival and health of the unit of all
living systems: the cell. "We're setting the foundation for reprogramming
healthy life," says study leader Valter Longo of the University of Southern
California.
Longo's group put baker's yeast on a calorie-restricted diet and knocked out
two genes - RAS2 and SCH9 - that promote aging in yeast and cancer in humans.
"We got a 10-fold life span extension that is, I think, the longest one that
has ever been achieved in any organism," Longo says. Normal yeast organisms
live about a week.
"I would say 10-fold is pretty significant," says Anna McCormick, chief of
the genetics and cell biology branch at the National Institute on Aging (NIA)
and Longo's program officer. The NIA funds such research in the hope of
extending healthy life span in humans through the development of drugs that
mimic the life-prolonging techniques used by Longo and others, McCormick
adds.
Baker's yeast is one of the most studied and best understood organisms at the
molecular and genetic level. Remarkably, in light of its simplicity, yeast
has led to the discovery of some of the most important genes and pathways
regulating aging and disease in mice and other mammals.
Longo's group next plans to further investigate life span extension in mice.
The group is already studying a human population in Ecuador with mutations
analogous to those described in yeast.
"People with two copies of the mutations have very small stature and other
defects," Longo says. "We are now identifying the relatives with only one
copy of the mutation, who are apparently normal. We hope that they will show
a reduced incidence of diseases and an extended life span."
Longo cautions that, as in the Ecuador case, longevity mutations tend to come
with severe growth deficits and other health problems. Finding drugs to
extend the human life span without side effects will not be easy.
I've always been a skeptic when it comes to life-extending research, but this
has me rethinking my position.
Lifespan Extension [PLoS Genetics]
Free full text at:
http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0040013
Life Span Extension by Calorie Restriction Depends on Rim15 and Transcription
Factors Downstream of Ras/PKA, Tor, and Sch9 Min Wei equal contributor,
Paola Fabrizio equal contributor,
Jia Hu,
Huanying Ge,
Chao Cheng,
Lei Li,
Valter D Longo mail
Abstract
Calorie restriction (CR), the only non-genetic intervention known to slow
aging and extend life span in organisms ranging from yeast to mice, has been
linked to the down-regulation of Tor, Akt, and Ras signaling. In this study,
we demonstrate that the serine/threonine kinase Rim15 is required for yeast
chronological life span extension caused by deficiencies in Ras2, Tor1, and
Sch9, and by calorie restriction. Deletion of stress resistance transcription
factors Gis1 and Msn2/4, which are positively regulated by Rim15, also caused
a major although not complete reversion of the effect of calorie restriction
on life span. The deletion of both RAS2 and the Akt and S6 kinase homolog
SCH9 in combination with calorie restriction caused a remarkable 10-fold life
span extension, which, surprisingly, was only partially reversed by the lack
of Rim15. These results indicate that the Ras/cAMP/PKA/Rim15/Msn2/4 and the
Tor/Sch9/Rim15/Gis1 pathways are major mediators of the calorie
restriction-dependent stress resistance and life span extension, although
additional mediators are involved. Notably, the anti-aging effect caused by
the inactivation of both pathways is much more potent than that caused by CR.
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