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DNA-damage or telomere shortening may not cause normal ageing


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.

Rapamycin fails to extend lifespan in telomerase-deficient mice, while improving lifespan by 39% in normal mice

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Bio-medical journal covering research on all aspects of gerontology

Mikhail Blagosklonny

Professor of oncology at the Roswell Park Cancer Institute

Roswell Park Comprehensive Cancer Center

First center in USA focused on cancer research and treatment