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.
| Evidence tier | C Animal in vivo |
| Study type | 4 - Animal Study |
| Model system | Genetically heterogeneous mice |
| Journal | Aging Cell |
| Year | 2012 |
| Peer reviewed | Yes |
| Source | DOI 10.1111/j.1474-9726.2012.00832.x · PMID 22587563 · Free full text (PMC3434687) |
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.
| Intervention | Rapamycin |
| Target | mTOR |
| Model | Genetically heterogeneous mice |
| Effect | Rapamycin slows multiple aspects of aging (heart, liver, tendon, activity), beyond just suppressing cancer |