Oliver's mTOR Atlas Evidence Platform
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Rapamycin slows aging in mice

Wilkinson JE, Burmeister L, Brooks SV, Chan CC, Friedline S, Harrison DE, Hejtmancik JF, Nadon N, Strong R, Wood LK, Woodward MA, Miller RA · 2012 · Aging Cell · Atlas ID WIL2012

What this study shows

Answered a crucial objection: does rapamycin really slow AGING, or just prevent the cancers that kill mice? By showing slower age-related change across many tissues (heart, liver, tendon, activity), it argued for genuine slowing of aging. Honestly reported harms too - more cataracts and testicular degeneration - making it a balanced landmark, not hype.

Abstract

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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.

Read the full abstract on PubMed →

At a glance

Evidence type A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Genetically heterogeneous mice); the code names the system studied -- animal work can be rigorous and still not be human data.
Study type4 - Animal Study
Model systemGenetically heterogeneous mice
JournalAging Cell
Year2012
Peer reviewedYes
Record last updated2026-08-22
SourceDOI 10.1111/j.1474-9726.2012.00832.x · PMID 22587563 · Free full text (PMC3434687)

Extracted findings

InterventionRapamycin
TargetmTOR
ModelGenetically heterogeneous mice
EffectRapamycin slows multiple aspects of aging (heart, liver, tendon, activity), beyond just suppressing cancer
Dose4.7, 14, or 42 ppm rapamycin in food, administered from age 9 months.
Sample sizeGenetically heterogeneous mice; young (4 month) and old (20-22 month) control groups, and old mice treated with rapamycin at 4.7, 14, or 42 ppm; N varies by outcome (e.g., 15-80 per group).
Effect sizeRapamycin significantly reduced incidences of liver degeneration (P=0.02), myocardial nuclear abnormalities (P=0.047), endometrial hyperplasia (P=0.05), and adrenal tumors (P=0.04); however, it increased cataract severity (P=0.014 males, P=0.001 females) and testicular degeneration (P<0.001).
LimitationsHistological evaluation of cataracts was limited to a small number of specimens; site-to-site variation was considerable for spontaneous activity; some observed trends did not reach statistical significance.

In the Atlas

Related topics

LongevityRapamycinmTORmTORC1

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Cite this paper

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Wilkinson, J. E., Burmeister, L., Brooks, S. V., Chan, C. C., Friedline, S., Harrison, D. E., Hejtmancik, J. F., Nadon, N., Strong, R., Wood, L. K., Woodward, M. A., & Miller, R. A. (2012). Rapamycin slows aging in mice. Aging Cell. https://doi.org/10.1111/j.1474-9726.2012.00832.x

@article{WIL2012,
  author       = {Wilkinson, J. E. and Burmeister, L. and Brooks, S. V. and Chan, C. C. and Friedline, S. and Harrison, D. E. and Hejtmancik, J. F. and Nadon, N. and Strong, R. and Wood, L. K. and Woodward, M. A. and Miller, R. A.},
  title        = {{Rapamycin slows aging in mice}},
  journal      = {Aging Cell},
  year         = {2012},
  doi          = {10.1111/j.1474-9726.2012.00832.x},
  note         = {PMID: 22587563},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper.

Barton, O. (2026). Oliver's mTOR Atlas (record WIL2012) [Data set]. https://mtor-atlas.org/study/WIL2012/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_WIL2012,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record WIL2012},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/WIL2012/},
  doi          = {10.5281/zenodo.22059963}
}