As a result of parabiosis research there is presently some interest in exploring transfer of blood from young donors and direct alteration of levels of circulating proteins to try to impact the progression of aging in the old. Making old blood more like young blood appears to reactivate dormant stem cell populations to some degree, and thus produce benefits due to increased tissue maintenance. At this stage it remains to be seen what else is happening under the hood, as well as what the cancer risk profile of doing this might be. Stem cell activity falters with age because it reduces cancer incidence, a part of the evolutionary trade off that enables we humans to live much longer than other primates.
In any case, here is an example of slowing aging via transfer of blood plasma, but the researchers are doing this in a breed of senescence-accelerated mice. So what is happening here might have some similarities to the case of young blood for old animals at the detail level - and here the researchers are looking at cellular senescence in particular - but it is really a situation in which researchers cause a specific narrow form of damage and then prevent some of the consequences of that damage by delivering functional biological parts. In all such studies the relevance to normal biology and normal aging is strained at best, and often there turns out to be no relevance. It is worth bearing in mind that a team did in fact recently conduct a blood transfusion study for young blood to old individuals in normal mice, and saw no benefit.
Aging is related to loss of functional stem cells accompanying loss of tissue and organ regeneration potentials. Previously, we demonstrated that the life span of ovariectomy-senescence accelerated mice (OVX-SAMP8) was significantly prolonged and similar to that of the congenic senescence-resistant strain of mice after platelet rich plasma (PRP)/embryonic fibroblast transplantation. The aim of this study is to investigate the potential of PRP for recovering cellular potential from senescence and then delaying animal aging.
We first examined whether stem cells would be senescent in aged mice compared to young mice. Primary adipose derived stem cells (ADSCs) and bone marrow derived stem cells (BMSCs) were harvested from young and aged mice, and found that cell senescence was strongly correlated to animal aging. Subsequently, we demonstrated that PRP could recover cell potential from senescence, such as promote cell growth (cell proliferation and colony formation), increase osteogenesis, decrease adipogenesis, restore cell senescence related markers and resist the oxidative stress in stem cells from aged mice.
The results also showed that PRP treatment in aged mice could delay mice aging as indicated by survival, body weight and aging phenotypes (behavior and gross morphology) in term of recovering the cellular potential of their stem cells compared to the results on aged control mice. In conclusion these findings showed that PRP has potential to delay aging through the recovery of stem cell senescence and could be used as an alternative medicine for tissue regeneration and future rejuvenation.