Key points from article :
Rapamycin fails to extend lifespan in DNA repair mutant and telomerase-knockout mice, while extending lifespan in normal mice.
Indicates neither DNA damage nor telomere shortening limits normal lifespan or causes normal aging.
In growth-retarded mice, rapamycin further retards weight gain.
Mikhail Blagosklonny, the author, mentions previous evidence:
- Overexpression of enzymes that decrease damage does not extend lifespan.
- Molecular damage and telomere shortening cannot reach a deadly threshold.
- Genetic knockout of signaling pathways extend lifespan without affecting damage.
- Intra- and inter-species differences in lifespan poorly correlate with rate of molecular damage.
- Nuclear transfer and nuclear reprogramming rule out DNA damage as a cause of aging.
- Molecular damage is not-life-limiting even when moderately increased.
- Rapamycin increases lifespan in normal animals, indicating mTORC1-dependent quasi-program is life-limiting.
Study by Roswell Park Cancer Institute published in Aging.
