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Sci. STKE, 10 October 2000
Vol. 2000, Issue 53, p. tw9
[DOI: 10.1126/stke.2000.53.tw9]


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.

Wolkow, C.A., Kimura, K.D., Lee, M.-S., and Ruvkun, G. (2000) Regulation of C. elegans life-span by insulinlike signaling in the nervous system. Science 290: 147-150. [Abstract] [Full Text]

Citation: Having the Nerve to Go On. Sci. STKE 2000, tw9 (2000).

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