Researchers are eager to understand the association of two biomarkers with the process of aging
Researchers are always eager to understand the processes that cause aging and disease. In one study, researchers tried to understand the role of two common biomarkers in aging.
The presence of the tumor suppressor protein called p16Ink4a, together with an enzyme produced by aging cells called β-galactosidase (SAβG), are commonly accepted as biomarkers of aging cells, called senescent cells (SCs). Recent reports attributed the improvement of the healthspan of aged mice to eradication of senescent cells that had these biomarkers.
While this association at first seemed to point to the presence of p16Ink4a/SAβG-positive white blood cells in dead tissue of old mice, indicating they could be considered biomarkers for aging, they also found it in the dead tissue surrounding the abdomen (in the peritoneal cavity) of young animals after they were injected with a negatively charged acid present in senescent cells. This raised alarm among scientists because they could not say that the presence of the biomarkers necessary indicates properties of aging.
This study was outlined in Aging Volume 9, Issue 8, in the article “p16(Ink4a) and senescence-associated β-galactosidase can be induced in macrophages as part of a reversible response to physiological stimuli.” These observations suggest that the anti-aging effects following eradication of p16Ink4a-positive cells may not be solely attributed to aging or senescent cells but also to non-senescent p16Ink4a/SAβG-positive white blood cells (macrophages).
The importance of this research lies in defining the exact purpose and nature of p16Ink4a-positive cells. It is crucial for proper development of therapeutics for the prevention and treatment of aging and age-related diseases. Today, the field of aging is focused on the development of small molecules that cause cell death (senolytic compounds), that are isolated for their ability to selectively kill senescent cell that are generated outside of the body, as in a lab. If these cells are different from p16Ink4a-positive cells that actually accumulate in the body with age, this could misdirect both academic studies of senescence as a phenomenon, as well as practical efforts to develop anti-aging therapeutics.
The motivation for this study was aimed at defining the nature of p16Ink4a-positive cells found in mouse tissues and determining their relation to the occurrence of cellular aging processes.