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Twenty First
Annual Darwin College Lecture Series
2006
Lecture 7 : 3 March
SURVIVING LONGER
Cynthia Kenyon
University of California, San Francisco
Abstract
Aging has long been assumed to be a passive consequence of
molecular wear and tear, counteracted by the force of natural
selection. But it's not so simple. Our discoveries have led
to the realization that the aging process, like everything else in
biology, is under exquisite regulation, in this case, by a complex,
multifaceted hormonal system that affects aging in many species,
including mammals. In 1993, we showed that changing a single gene in
the small roundworm C. elegans can double its lifespan. This gene
encodes an insulin/IGF-1 like receptor, which indicates that aging is
regulated hormonally. By manipulating genes and cells, we have now
been able to extend the lifespan and period of youthfulness of
C. elegans by six times. We have found that signals from the
reproductive system and sensory neurons influence lifespan. These
signals act, at least in part, to control inslin/IGF-1 hormone
signaling. These hormones influence the lifespan of the animal by
coordinating the expression of a wide variety of subordinate genes,
including antioxidant, stress response, antimicrobial, and novel
genes, whose activities act in a cumulative fashion to determine the
lifespan of the animal. Some of these subordinate genes can also
influence the rate of onset of age-related disease. In this way, this
hormone system couples the natural aging process to age-related
disease susceptibility.
The lectures are given at 5.30 p.m. in The Lady Mitchell Hall,
Sidgwick Avenue, with an adjacent overflow theatre with live TV
coverage. Each lecture is typically attended by 600 people so you
must arrive early to ensure a place.
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