Rapamycin slows aging in mice

John E. Wilkinson(University of Michigan), Lisa Burmeister(University of Michigan), Susan V. Brooks(University of Michigan), Chi‐Chao Chan(National Institutes of Health), Sabrina Friedline(University of Michigan), David E. Harrison(Jackson Laboratory), J. Fielding Hejtmancik(National Institutes of Health), Nancy L. Nadon(National Institutes of Health), Randy Strong(The University of Texas at San Antonio Health Science Center), Lauren K. Wood(University of Michigan), Maria A. Woodward(W.K. Kellogg Foundation), Richard A. Miller(University of Michigan)
Aging Cell
May 15, 2012
Cited by 684Open Access
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Abstract

Rapamycin increases lifespan in mice, but whether this represents merely inhibition of lethal neoplastic diseases, or an overall slowing in multiple aspects of aging is currently unclear. We report here that many forms of age-dependent change, including alterations in heart, liver, adrenal glands, endometrium, and tendon, as well as age-dependent decline in spontaneous activity, occur more slowly in rapamycin-treated mice, suggesting strongly that rapamycin retards multiple aspects of aging in mice, in addition to any beneficial effects it may have on neoplastic disease. We also note, however, that mice treated with rapamycin starting at 9 months of age have significantly higher incidence of testicular degeneration and cataracts; harmful effects of this kind will guide further studies on timing, dosage, and tissue-specific actions of rapamycin relevant to the development of clinically useful inhibitors of TOR action.


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