X-Message-Number: 16009
From: Brent Thomas <>
Subject: new hormone related aging system identified.
Date: Fri, 6 Apr 2001 09:44:33 -0400 

hmmm...this could lead in short order to a better understanding
of (at least one of) the aging mechanism(s). It seems like a pathway that
would be amenable to detailed experimentation and study.

from http://www.sciencedaily.com/releases/2001/04/010406074352.htm

Researchers Find Evidence Of Aging System
         That May Promote Long Life 

         PROVIDENCE, R.I. - Scientists have provided the first evidence of a
         hormone-based aging mechanism they suggest may promote long life in
         species ranging from roundworms to humans. The mechanism begins in
         the brain with a mutant gene that suppresses the release of
hormones that
         prompt rapid aging. 

         "This is the first evidence of the way this aging mechanism works,"
said
         lead investigator Marc Tatar, of Brown University. "It appears that
aging
         is hormonally regulated, with a brain-based pathway that affects
general
         hormones that come from a pituitary-like system." 

         The researchers studied a gene with function in the brain and other
cells,
         called an insulin-like receptor (InR). The gene is analogous to
those in
         species from top to bottom of the animal kingdom. 

         Fly InR responds to a form of insulin. As a result, brain cells
tell a thyroid-
         or pituitary-like system to release a second hormone called
juvenile
         hormone. This compound circulates in the body, unleashing a chain
of
         other events that trigger reproduction and rapid aging. 

         The researchers bred fruit flies with mutant InR. They believed the
         mutation suppressed the release of juvenile hormone, arresting the
aging
         process. Indeed, the breeding experiment produced dwarf females
with life
         spans extended by up to 85 percent. Dwarf males also resulted, but
they
         were generally frail and most died by 20 days. Males that survived
to 20
         days had low subsequent death rates. 

         To test whether mutant InR had suppressed juvenile hormone, the
         researchers administered juvenile hormone to treat the long-lived
flies. The
         treatment restored typical life expectancy to the insects. 

         In the brain, an important aging function is taking place, which
plays a
         powerful role in the rest of the body, the scientists said. Their
study
         appears in the current issue of Science. 

         "We concluded that juvenile hormone deficiency, which results from
         mutation in the insulin-like receptor pathway, is sufficient to
extend
         lifespan," said Tatar, assistant professor of ecology and
evolutionary
         biology. "We think that in flies and worms, and probably in humans,
         insulin-like compounds mediate aging by either retarding growth or
by
         activating specific endocrine tissue to release other hormones." 

         Scientists may guess which hormones may be involved in human aging,
         "but we don't know which brain signals or external environmental
signals
         turn on the aging mechanism," he said. "This aging mechanism is
         something we don't understand at all in humans. But we know
something
         is going on. The neurocircuitry in our brains is similar to that of
flies." 

         Aging is much easier to study in flies than in humans, Tatar said.
As
         cold-blooded creatures, flies have a much greater range of
adaptability to
         environmental signals such as light, temperature or food. These all
may
         trigger reproduction and rapid aging. 

         "Our brains function in a narrow range of physiological states and
perhaps
         cannot adapt to signals that in cold-blooded organisms may prompt
         long-lived states," he said. "Humans don't adapt to environments.
We
         adapt environments to us." 

         The research serves as a model for further studies in other species
such as
         mice, where scientists already breed all sorts of genetic
possibilities, Tatar
         said. He and colleagues are currently studying how a fly brain
makes
         insulin and how the insulin-signaling pathway regulates hormones
that
         circulate throughout the body. 

         "We'd also like to study how juvenile hormone regulates body
aging,"
         Tatar said. "What does it do to tissues and cells, for example?
Does it
         increase a fly's resistance to stress or change a fly's immune
resistance?" 

         Co-author Robert Garofalo, now of Pfizer Global Research and
         Development, originally isolated the mutant gene in fruit flies,
while on the
         faculty of SUNY Downstate Medical Center. Garofalo had studied
         diabetes by looking into insulin receptor function. He and
colleagues
         developed fruit flies with mutations in their insulin receptors.
They found
         that this mutation limited the flies' growth and rendered them
infertile. 

         The other authors are former Brown undergraduate Andrew Kopelman;
         current Brown undergraduate Diana Epstein; post-doctoral researcher
         Meng-Ping Tu, who conducted the research as a graduate student at
the
         University of Massachusetts; and faculty member Chich-Ming Yin,
         University of Massachusetts. 

         The research was funded by a grant from the National Institute of
Aging
         and a New Scholar Award from the Ellison Medical Foundation. 

         Editor's Note: The original news release can be found at
         http://www.brown.edu/Administration/News_Bureau/2000-01/00-108.ht

Brent Thomas

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