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Comment by JohnJamesRambo | Hacker News Reader

Why did they use the mice with the progeria gene? Wouldn't the results be more impressive in wild-type mice? Were they just trying to get around the 2-3 year lifespan of a lab mouse faster?

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Oh they did, in fact, but the results in WT mice were not as easy to overhype. The effects were extremely minor to nonexistent in aged wild-type animals (Fig S7 from the paper). Unfortunately, press releases and the subsequent news articles -- as usual -- have totally oversold what this paper means.

So what you're saying is that the mice that didn't have their genome edited didn't have a drastic life extension? I assume the improvements only occurred in the mice that had their genomes edited to reduce Yamanaka factors because they then artificially replaced the Yamanaka factors?

No. That's not quite what I'm saying. There was no particularly interesting effect of inducing transient expression of the Yamanaka factors on normal mice reported in this paper. It is effectively a negative result that's being reported, as it pertains to wild-type mice.

The paper primarily reports results that pertain to mice with a genetic defect that causes progeria. Mice with this defect have a shorter-than-normal lifespan.

so its more a treatment for progeria than general aging reversal

I had the same thought. This puts an asterisk on the integrity of the report IMHO.

Doxycycline has also been shown to greatly increase life expectancy! Of patients currently suffering from bacterial infection.

Yes and tetracyclines like doxycycline affect mitochondrial function and may confound the research in that way too.

http://dx.doi.org/10.1016/j.celrep.2015.02.034

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