Here's a long and detailed post from the SENS Foundation on the recent demonstration of the benefits of senescent cell destruction: "studies involving the use of putative 'premature aging' models must be interpreted with caution ... In the case of this new report, however, while caution is still merited, the nature of the intervention used makes the study relatively free of such complications. The investigators did not simply modulate or normalize the very thing that the mutation (in this case, to the mitotic checkpoint component BubR1) itself disrupts, as in other widely-publicized studies involving putative 'accelerated aging'. Rather, the defective checkpoint system was left to proceed, and one of its downstream consequences, which was still under normal regulation - and one known to be directly induced by the normal degenerative aging process - was reversed at the structural level, by clearing out the p16Ink4a-positive senescent cells that had accumulated to an abnormal degree in their tissues. This left some aspects of the abnormal 'progeroid' phenotype in these organisms (the cardiovascular defects) intact, but illustrated the dysfunctional consequences of having tissues riddles with such cells. While still of abnormal origin, there is no strong reason to think that the ongoing effects of a rising burden of such cells would not be similar - and thus, that the effects of ablating such cells are uninformative about the effects of a similar intervention in 'normally' aging bodies. ... How might the results of this intervention be translated for human rejuvenation therapies? ... SENS Foundation is currently funding work by Dr. Kevin Perrot in Campisi's laboratory, screening compounds for their effectiveness in eliminating cells exhibiting the classical senescence-associated secretory phenotype."