Sci. STKE, 10 October 2000
Aging Having the Nerve to Go On
In the nematode Caenorhabditis elegans, mutations that disrupt the signaling pathway of the insulin-like receptor daf-2 dramatically extend the animals' life-span and cause the accumulation of large amounts of fat. By selectively expressing normal versions of the mutated insulin-like receptors only in certain tissues, Wolkow et al. pinpoint the nervous system as responsible for this pathway's effect on life-span and the muscles, as the site that controls the metabolic alterations. The authors suggest that defects in the daf-2 pathway allow overexpression of free-radical scavenging enzymes, which protects neurons from oxidative damage and allows them to secrete life-prolonging neuroendocrine signals.
Citation: Having the Nerve to Go On. Sci. STKE 2000, tw9 (2000).
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