Old Blood Versus Young Blood From a Programmed Aging Perspective

The programmed aging camp points to experiments such as this as supportive of their view that aging is a genetic program that gives rise to damage and change, rather than resulting from damage that causes epigenetic changes to arise in reaction. The data could be interpreted either way, however, and there are other reasons to believe that aging is caused by damage:

In a 2005 experiment, one old mouse and one young mouse became artificial Siamese twins. For control, [researchers] also paired two old mice and two young mice. After the surgery, they injured one mouse from each pair, and monitored the healing process at a cellular level. As expected, the young mice recovered from injury much more efficiently than old mice. The surprise was that old mice that were paired with young mice healed as if they were young. "Importantly, the enhanced regeneration of aged muscle was due almost exclusively to the activation of resident, aged progenitor cells, not to the engraftment of circulating progenitor cells from the young partner." In other words, it was not young cells that implanted themselves in the old mice; it was signal proteins in the blood that told the old mouse tissue to go ahead and heal as if it were young.

[A recent paper] culminates in a proposal for whole-body rejuvenation that might be practical in the near term. Fortuitously, its safety in humans has already been established, so people might be willing to try it if a course of animal experiments shows promise. The idea is simply to transfuse older subjects with blood plasma from a young donor, repeated often enough to sustain levels of signaling proteins that control gene expression.

The mainstream view on why stem cells and tissue maintenance decline with age is that it is an evolved response to rising levels of damage that reduces cancer risk. Flooding an old system with young signaling overrides that response, but would probably be accompanied by an increased risk of cancer - though in the case of a short-term signal change as a therapy to promote regeneration of a specific injury, that may be an acceptable risk. In the long term, however, the underlying damage has to be repaired, rather than just forcing our biochemistry to continue as though it didn't exist.

Link: http://joshmitteldorf.scienceblog.com/2013/03/25/young-blood/


Its true there may be an increase in the cancer rate, but wouldn't the immune system also be restored increasing our defences against cancer?
Similar fears are held for telomere activators, but it doesn't appear that those fears are justified.

I imagine that before the "young plasma " growth factors would be completely successful you would have to find a way to remove or inhibit "old plasma" factors.


Posted by: Mike at April 2nd, 2013 4:21 PM

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