Reports coming from Stanford University School of Medicine and Harvard Medical School are leading to speculation that scientists have discovered a blood protein holds the key to reversing the damage caused by growing old.
The protein is one of a group of proteins known to be regulators of cell growth and differentiation in both embryonic and adult tissues.
Its official full name is growth differentiation factor 11 (GDF11) and its presence in blood is known to decline throughout life.
The recent results builds on centuries of thought that the blood of young people contains something that could rejuvenate an old person.
The modern research began in the 1950s with researchers at Cornell University connecting the circulatory system of a young mouse with an old mouse.
Remarkably, as the blood of the young mouse began to circulate in the old mouse transformations took place that the scientists realised were worthy of further investigation.
Continuation of this work was taking place while by the early 2000s stem cell research at many research centers worldwide had firmly established that stem cells are essential for repairing damaged tissue.
That led to numerous studies showing astounding success in producing human tissue from stem cells.
Already there are some fortunate human patients who have received windpipes or bladders built from their own stem cells in a process named tissue engineering.
With those early successes there is a frontier process taking place where there is anticipation that tissue engineering will be able to produce kidneys, livers, arteries, hearts and more.
Since they could be made from a person's own stem cells harvested from the person's bone marrow and multiplied outside the body the transplant of such tissues into a patient would not cause an immune reaction since essentially they would be the patient's own tissue.
While that work was going on scientist were rethinking prior ideas on what happens to the body as we age.
It was thought originally that stem cells were dying off and declining in numbers so that repairs were slower and less efficient.
But then it became clear that stem cells were not dying off to the extent that had been thought but instead were not being activated as much as they were in a young person.
Another look at the linking of the circulations of an old mouse with a young mouse revealed that as the old mouse exhibited changes typical of a young mouse the reverse happened in the young mouse.
Further investigation revealed that the GDF11 protein in mice was abundant in young mice and low in old mice.
The next step was to produce a supply of mouse GDF11 and inject it into an old mouse.
The results were astounding.
It revived stem cells in the old mouse with the anticipated renewal of muscle tissue.
By 2011 new studies showed that plasma from young mice initiates the growth of blood vessels and neurons in the brain of old mice.
All the different research groups are in agreement on the effects being found with restoring youthful GDF11 levels.
The implications for humans is astonishing.
Although the mouse work still needs more investigation some researchers are already planning to apply for approval to begin human clinical trials with human GDF11 in the near future.
It is likely that injection of human GDF11 into patient's with Alzheimer's disease could be approved within the next couple of years.
Where this could lead is no longer an ancient dream.
Practical plans are being made.
Some are speculating on a very long healthy longevity.
I urge you to search for articles on GDF11 and read about the many different researchers working on this frontiers.
It must be an exciting time for the young people working in their research buildings.
It's a remarkable time for older people who may benefit from the work they are doing.