A shared mechanism for lifespan extension by rapamycin, acarbose, and 17α-estradiol

An interesting paper, I was surprised by the shared pathway… suggests that dosing all of them won’t bring additional benefits, perhaps, but the recent good rapa / acarbose results suggest there are other pathways also…

Diminution of mTORC1 activity and increases in CIT-dependent proteins may represent a shared pathway for both long-lived-mutant mice and drug-induced lifespan extension in mice.

Full Text Paper Here: Cap‐independent translation: A shared mechanism for lifespan extension by rapamycin, acarbose, and 17α‐estradiol - PMC

Pubmed Summary Here:

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As I understand it, most protein translation in the ribosome is dependent on an RNA capped at its end. But there are also translation points internally on the RNA that are uncapped and less efficient, and this is called cap-independent translation.

The article is saying that the 3 drugs all reduce mTORC1 and cap-dependent protein translation, but they increase age-related declines in cap-independent translation. Correct?

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