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For the first time: Longevity modulated without disrupting life-sustaining function

Within a hormone-triggered cascade of molecular signals that plays a crucial for a wide range of physiological functions, researchers for the very first time have identified a protein that functions specifically to extend lifespan and youthfulness -- without disrupting fertility, immunity or the organism's response to stress.

"In past experiments, meddling with this versatile pathway to exploit its beneficial effects on aging and life span inevitably invited a host of problems," says Andrew Dillin, Ph.D., an assistant professor in the Molecular and Cell Biology Laboratory at the Salk Institute for Biological Studies and leader of the study, reported in the March 9 issue of the journal Cell.

The Salk scientists discovered the protein in studies with worms, a commonly used lab model in genetics; since this signaling cascade including the newly identified protein is conserved across many species, including humans, these findings raise the prospect that one day it might be possible to medically tweak this pathway to slow aging and improve the quality of life without harmful consequences to the body.

In humans and other mammals this signaling cascade is known as the insulin/IGF-1 pathway since it is prompted by insulin and the closely related insulin-like growth factor-1 or IGF-1. IGF-1 is the main trigger for childhood growth but continues to exert growth stimulating effects throughout an individual's life. Insulin, which is best know for controlling blood glucose levels, has additional and equally important regulatory functions in the body. In worms, however, the chain of signals is set in motion when a single receptor on the cell surface is matched to an insulin-like signal.

"If you were to interfere with insulin signaling in humans in order to prolong life, you would induce diabetes right away," cautioned graduate student and first author Suzanne Wolff. When this pathway had been clipped in worms, they lived longer than normal, but th
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Source:Salk Institute


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