Yeah, perhaps. But if the genetic defect just makes the decay appear earlier but same mechanism, it may still be useful??
On Sat, Jan 5, 2013 at 7:19 PM, Cathal Garvey <cathalgarvey@gmail.com> wrote:
The punchline that they lived 150% longer seems to be based on the shortened lifespan of the mouse strain used, too. If so, it's pretty unimpressive; they are correcting for a genetic defect that leads to early death by complementing with new stem cells. Very useful data for person suffering similar conditions, but I don't see that it has any relevance to normal ageing, I'm sorry to say.
On 23 December 2012 20:26, jlund256 <jlund256@gmail.com> wrote:The model mice used have a mutation that kills fast dividing cells off. Stem cells are cells that divide fast and often, so this kills off stem cells, and this produces (through poorly understood mechanisms) premature aging and early death.
So it is not super surprising that a stem cell treatment would partially correct that. The interesting part is that the stem cells provided in the treatment could find their way to the stem cell niches in the mice, and then take on the local stem cell type and contribute to local tissues.
What does this mean for normal aging? Can stem cells partially reverse it? I'm not up to date on the literature, but certainly injecting stems has been tried and failed in experiments in many labs. So while it is interesting that there are positive results in this paper, simply repeating it in old mice is unlikely to work.
The interesting bit is that is had some effect in this very artificial model, and if the result holds up, it can be used to investigate why it works in progeria model mice but not in old mice. Was it the type or stem cells, or how they were delivered, or are the progeria model mice receptive in a way that old normal mice are not?
Jim LundTo view this discussion on the web visit https://groups.google.com/d/msg/diybio/-/if-zaCZnvCAJ.
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