A recent study, published in Aging Cell, found that blood cells could hold the key to aging. In a study, scientists found human blood cells have an intrinsic clock which remains steady even after the transplant. They say the clock could control human aging and may cause blood cancers.
The international team of researchers studied this master clock. Thus, the research team measured the cellular age in blood cells which were transplanted from healthy donors to leukemia patients. This was done by focusing on donor-recipient pairs of very different ages.
According to the researchers, this study is related to the fountain of youth. They found that young blood cells stay young in older people. However, there was no faster aging of young blood cells in an older human body.
Moreover, the research team found that the other direction was also true, blood cells from adult donors moved to a child stay older. The cells retained their intrinsic age approximately two decades after the transplant.
Their inherent stability proposes that the blood cells are not easily influenced by their environment. So, they could be the master clock of human aging.
Findings of the study
Thus, the study exposed that blood cells hold epigenetic patterns in DNA methylation, chemical groups attached to DNA, which can be used to estimate their age.
In spite of considerable age differences between donor and recipient (equal to 49 years), the DNA methylation age of transplanted blood indicated the age of the donor, even after years of contact to the recipient’s body. Researchers found that DNA functions as a timekeeper of our age.
DNA methylation as age predictor was first described in 2013. They found that the formula, the mechanism, and whether body cells synchronize DNA methylation age, wasn’t clear.
Researchers tested blood samples. These samples were collected regularly as part of transplant monitoring, with support from the Case Comprehensive Cancer Center.
One of the researchers expanded his sample source through leukemia researchers at the University of Oslo, in Norway. He crunched cellular ages via 353 distinct methylation sites found on blood cell DNA.
Together, the scientists provided the first experimental evidence that the aging clock of blood cells is an intrinsic factor of the cell. And not set by interactions with other cell types.
Researchers are now working for the identification of mechanisms which can change the clock. The clock is broken in cancer cells. As, patterns of DNA methylation are unstable in cancerous blood cells and frequently show odd aging –200 or 5 years old in a 50-year-old patient, for instance.
It does not match with the real age at all. Researchers caution that this is the reason, though it may sound interesting, they don’t yet recommend “therapeutic” cell infusions to try to maintain youth.
Instead, researchers are working to comprehend why epigenetic age differences occur in cancer cells, and how they could be overwhelmed. Also, they found that it may be by turning on or off certain genes within the cells, we can reset the clock.
Current studies show the DNA age of cells can be used as a biomarker for the prediction of the age-associated disease risk, like cardiovascular disease, Alzheimer’s disease, and others. Last year, researchers published an article reporting that DNA age is meaningfully accelerated in Progeria patients suffering from premature aging.
Researchers now have many studies ongoing to reveal the mechanism of age-dependent DNA methylation and to know how factors like exercise, diet, and oxygen levels affect epigenetic clocks.