Hmmm.... I know some people that would volunteer to be
test subjects in an experiment on humans... *grins*
--- Xiaoguang Li <firstname.lastname@example.org> wrote:
> ---------- Forwarded message ----------
> Date: Wed, 23 Feb 2000 19:10:33 PST
> From: "UPI / LIDIA WASOWICZ, UPI Science Writer"
> Newsgroups: clari.tw.science, clari.tw.top,
> clari.tw, clari.tw.misc,
> Subject: Molecule slows aging by silencing genes
> By LIDIA WASOWICZ, UPI Science Writer
> SAN FRANCISCO, Feb. 23 (UPI) -- Scientists who have
> the secret of a protein molecule that can slow aging
> in yeast by turning
> off selected sections of its genetic machinery want
> to know whether the
> same key could open the door to longer lifespans for
> men and women.
> "The hope is that researchers may one day be able
> to intervene
> in, and possibly inhibit, the aging process in
> humans," said lead study
> author Leonard Guarente, professor of biology at the
> Institute of Technology in Cambridge.
> While much work remains, including a corroboration
> of the
> results in animals, "our findings keep this hope
> alive," he told United
> Press International.
> The research may provide the missing link that ties
> previous results showing that yeast with extra
> copies of the protein
> Silent Information Regulator, SIR2, live longer,
> that decreased metabolic
> rates extend longevity and that cutting back on
> calories slows metabolism
> and adds years to one's life.
> "The new finding connects longevity, the silencing
> of gene
> expression and the slowing of metabolic state,"
> Guarente said in an
> Studies have shown reducing caloric intake can
> lifespan, although the mechanism for this
> correlation has been unclear,
> the scientists said in the British journal Nature.
> SIR2 might be the link
> between energy metabolism and longevity, turning
> genes off in response to
> reduced energy levels, they suggested.
> "So far, we have shown the connection between
> silencing and
> longevity in yeast, a simple system. The silencing
> is keeping the genome
> stable; it is genome instability that causes aging,"
> Guarente said. "We
> don't know if this is true in humans."
> Before the year is out, the investigators expect to
> gained key insight into whether SIR2 controls aging
> in animals, notably
> mice, which normally live two to three years, and
> worms, with a
> two-to-three-week lifespan. They plan to insert an
> extra copy of SIR2 in
> the animals to determine if it will enable them to
> live longer.
> "With the worm's short longevity, especially, we
> can get a
> view of the aging picture rapidly," Guarente said.
> "If we find SIR2
> regulates aging in animals, we will know we are on
> Any success in slowing the aging process will have
> far-reaching repercussions on human health, the
> scientists said.
> "If we slow down aging, we will slow down the
> diseases closely
> associated with aging, such as osteoporosis. The
> whole point would be to
> reduce the period of morbidity," Guarente said.
> "Does this mean we could be immortal? No, but it
> does mean
> some of the diseases of aging could be curtailed so
> that we could play
> tennis and feel healthier and lead more active lives
> If the animal tests corroborate the early findings,
> the next
> phase would be to design an anti-aging drug and to
> test it on worms, he
> said, emphasizing any such pill would slow down --
> not reverse -- the
> aging process.
> "Our goals are very much in the spirit of modern
> medicine --
> to increase the human health span," Guarente said.
> In the yeast experiment, the researchers found the
> enzyme has its spell-binding effect by turning off
> entire sections of the
> genome, the complete set of an organism's genes,
> said study co-author
> Shin-ichiro Imai, postdoctoral associate in biology.
> The study gives scientists a better understanding
> of previous
> findings that restricting caloric intake to 70
> percent of normal levels
> significantly extends the lifespans of yeast,
> earthworms, mice and
> possibly primates, the authors said.
> "This is the first concrete indication that genome
> and metabolism are connected," Guarente said.
> Proteins related to SIR2, discovered in the yeast
> Saccharomyces cerevisiae -- where it is involved in
> turning off genes --
> have been found in mammals, including man, the
> scientists said. What
> remains to be seen is whether adding extra copies of
> the molecule to the
> higher lifeforms will produce the same
> life-extending results it did in
> the simple system.
> The team discovered SIR2 is a type of histone
> deacetylase, an
> enzyme which turns off gene production by modifying
> the so-called
> "chromatin" proteins, those that package and protect
> thread-like structures that transmit genetic
> inheritance from parent to
> In each cell, some genes are active and others
> silenced. Skin
> and brain cells, for example, are genetically
> identical -- the difference
> lies in their prebirth programming to produce
> certain genes but not
> others. SIR2 can influence which gene groups are
> permanently silenced,
> the end result being prevention of age-related
> problems that surface late
> in life, the scientists said.
> "As cells age, genes that had always been turned
> off sometimes
> get turned on, causing problems that can lead to
> cell death," Guarente
> said, noting SIR2 would prevent such activation.
> To their surprise, the scientists observed that to
> carry out
> its life-prolonging function, SIR2 requires the
> ubiquitous energy carrier
> nicotinamide adenine dinucleotide, or NAD, which is
> normally involved in
> the breakdown of food molecules, said study
> co-author Christopher
> Made by all cells, these co-enzymes help transfer
> and hydrogen in some reactions that reduce
> oxidation, said study
> co-author Matt Kaeberlein, noting studies have
> linked food high in
> anti-oxidants to lower cancer rates and slowed
> "Although NAD and NADH are frequent enzyme
> co-factors in
> oxidation-reduction reactions, this is the first
> example to our knowledge
> in which NAD drives a distinct enzymatic reaction,"
> the authors wrote.
> "The NAD connection came out of the blue, but it
> has an
> interesting implication: NAD could well be the
> signal for the metabolic
> status of cells," Guarente said. "If an organism is
> starved for calories,
> the NAD level may go up. More NAD means activating
> SIR2, which silences
> sections of the genome and increases lifespan."
> Since genes similar to SIR2 have been found in
> organisms, Guarente said, the hope is "if we can
> keep SIR2 active for
> longer, we may slow down aging."
> The research was funded by the Human Frontier
> Science Program
> Organization, the National Institutes of Health, the
> Seaver Foundation,
> Ellison Medical Foundation and the Howard and Linda
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