The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
the basic idea that knocking down to our complex one might be a good thing and that knocking down tor complex two might be a bad thing that was the premise of your question i think that's a good initial sound foundation for further work but the interactions between them the ways in which different cell types may have different responses it's going to be much more complicated than that
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this raises the possibility that is actually the elevation of tor complex ii in these mutant mice it's good for them and gonzalo has found several examples of mice where there's a mutation that blocks the mtar complex ii elevation they do not live a long time
from the perspective of aging biology people have focused almost exclusively on mtor complex 1. there's a little bit of data in c elegans on mtor complex 2 affecting lifespan but outside of c elegans almost all of the data for rapamycin or mtor as a regulator of aging is thought to be mediated by inhibition or reduced signaling through mtor complex one