Sirtuins (such as Sir2 in yeast or Sirt1 in mammals) are in the news again; a set of releases and a new paper in the past few days on research into sirtuin inhibitors. I imagine that this research has been proceeding at a slow pace for a while and suddenly became hot when it was realized that, contrary to previous findings, inhibiting rather than enhancing sirtuins may a much better path to an extended healthy life span through metabolic manipulation. The biochemistry is more complex than one might have thought - which really should be no surprise to anyone who watches biomedical research - and the present state of knowledge is rapidly changing and evolving. With that in mind, I should point out a post on this topic from In the Pipeline that I missed last month:
The big question now, given all these divergent cell findings, is: will these guys live longer, or not? And what happens to them when you put them on a limited-calorie diet? Are they going to act like the replicative-aging models, or the chronological aging ones? (We'll leave the yeast-mouse contradiction out of it for a while). Perhaps the two mechanisms will fight each other to a standstill, leaving the animals with plain ol' normal lifespans, but with some tissues acting much younger than the whole-body age and some acting much older. Mice generally live around two years. I wonder just how many months ago these lifespan studies started. . .
In any case, it's encouraging to see that research, in this field at least, has diversified to the point that promising work on potential sirtuin inhibitors was accomplished and ready to go in advance of the need. I'll momentarily put aside my skepticism regarding the potential of healthy life extension resulting from metabolic tinkering to note that I'm sure we'll see some very interesting mouse longevity experiments over the next few years - especially given that $3 million incentive to beat the present record.