The mice used in this study are a breed engineered to suffer accelerated aging, which means it doesn't have too much to say about what will happen in normal mic

The mice used in this study are a breed engineered to suffer accelerated aging, which means it doesn't have too much to say about what will happen in normal mice: this study adds weight to arguments for the importance of senescent cells in aging by virtue of the degree of change that was produced. To my eyes, the important outcome here is the development of a reliable way to flush out senescent cells in mice - which can now be applied to otherwise normal mice to see what happens there. Will they live longer, what will their risk of age-related disease be, etc? For further reading on senescent cells, see: http://www.fightaging.org/archives/2008/06/why-do-we-accumulate-senescent-cells-anyway.php http://www.fightaging.org/archives/2008/06/why-do-we-accumul... For commentary on this research: http://www.fightaging.org/archives/2011/11/a-demonstration-of-the-merits-of-apoptosens.php http://www.fightaging.org/archives/2011/11/a-demonstration-o... The paper: http://dx.doi.org/10.1038/nature10600 http://dx.doi.org/10.1038/nature10600 "Senescent cells accumulate in various tissues and organs with ageing and have been hypothesized to disrupt tissue structure and function because of the components they secrete. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16Ink4a, to design a novel transgene, INK-ATTAC, for inducible elimination of p16Ink4a-positive senescent cells upon administration of a drug." Running this method in otherwise normal mice rather than the BubR1 accelerated aging mice used here will be an important test of the merits of research programs like the SENS Foundation's apoptoSENS: http://sens.org/sens-research/research-themes/apoptosens http://sens.org/sens-research/research-themes/apoptosens But it will be at least another five years, I'd imagine, to get the results of a life span study in ordinary mice, even if they turn right around and start pulling down the grants right now. The BubR1 mutant progeria-suffering mice used in this work are discussed in a good article at the lab website: http://discoverysedge.mayo.edu/de07-2-aging-vandeursen/index.cfm http://discoverysedge.mayo.edu/de07-2-aging-vandeursen/index...