...senescent cells...reliably switch on a characteristic marker gene known as p16-Ink4a. [Barker et al.]... arranged that the genetic element that switches on the marker gene would also prime a mechanism to make the cell self-destruct. The mechanism fired only when the mice were dosed with a specific drug. The result was that only senescent cells were at risk from the drug...they could be purged at any desired time in the mouse’s lifetime.Life-long removal of senescent cells delayed the onset of age-related pathologies in fat,skeletal muscle, and eye tissues, and clearance in late life attenuated the progression of these pathologies (such as cataracts). So, it appears that removal of senescent cells can prevent or delay tissue dysfunction and should extend lifespan.
Wednesday, December 07, 2011
Purging senescent cells can prevent some ills of aging.
I've held off on noting some recent work relevant to longevity that has received quite a lot of press, because I increasingly rebel at the enormous amount of effort going into life extension. It is hard, however, to not be interested in experiments that appear relevant to enhancing the quality of a normal life span, so that health and robustness are maintained until a system failure rapidly takes down the whole show. The report by Baker et al. examines cells that have stopped dividing (senescent cells) and hasten aging in the tissues in which they accumulate (like my arthritic knees!) by secreting agents that stimulate low-level inflammation. Barker et al. use a neat genetic trick (not yet available to us humans) to eliminate senescent cells in mice. From Wade's summary: