Millions of years ago, humans became aware of the existence of immortality. Since then, their quest to achieve it has not ceased. Pursuing eternal life is nothing but a way of trying to overcome the anguish of lurking death. Aging and its effects are the main cause of this fear. Today, science is working toward achieving a clear goal: delaying the decline and depletion of our cells, since they are the ones responsible for showing the outside signs of aging.
Just weeks ago, scientists at the Salk Institute for Biological Studies in California, managed to achieve a 30% increase in life expectancy in mice, rejuvenating their appearance by transforming normal cells into pluripotent stem cells, without losing their identity. They have thus managed to influence the aging process that is the biggest risk factor for developing cardiovascular disease, various cancers and neurodegenerative disorders. A new door of hope for the human being is so opened. It is predicted not only to get humans to live more years, but to do so with a better quality of life.
Telomerase: a silent protagonist
Few molecules have been studied by the scientific community in recent decades more than the telomerase, an enzyme formed by a complex ribonucleoprotein with polymerase activity that enables the telomeres to be elongated. Although the protective function of telomeres was already described in the early thirties by scientists Barbara McClintock and Hermann Müller[1], Telomerase had to wait until 1985 to be discovered by Carol Greider and Elizabeth Blackburn, who would receive the Nobel Prize in 2009.
The Karolinska Institute described its work as a direct form of “shedding light on the mechanisms of disease and stimulating the development of potential new therapies.”
The Karolinska Institute described its work as a direct form of “shedding light on the mechanisms of disease and stimulating the development of potential new therapies.”
Today we know, among other things, that telomerase has the ability to keep telomere length steady and even repair and lengthen those telomeres that are critically short. Telomerase is found in all cells, including cancerous cells, where after successive divisions, no telomere shortening is observed. Cells therefore become practically immortal. In addition, science has been able to determine how shorter telomeres are more decisively contributing to the development of different types of diseases. These include cardiovascular disease, type 2 diabetes, pulmonary fibrosis and depressive disorders, among many others.
The measurement of telomeres: the key to personalized medicine
As a result of this research on mice, and other publications over the years, the incorporation of evidence relating to the measurement of telomeres by physicians, is growing exponentially. In turn, we are finding a growing demand by patients, who are increasingly aware and concerned about delaying the aging process. In this context, various kinds of tests have been developed and marketed that quantify, compare and analyze, not only the length of telomeres, but also determine those that are critically short, and which are key to defining the overall health of each individual cell.
One of the main conclusions drawn from research developed in this field is that the study of telomeres is a key biomarker in early identification of disease, as it will make it possible to stratify its risk and prescribe treatments against it at the right time. In addition, from an initial measurement it is possible to carry out actions to limit cell damage in the future. The idea is to achieve changes in patients: in their lifestyles, their diet or the impact of the environment in which they undertake their daily activities.
How telomeres are measured and what they are used for
Undoubtedly, the greatest value provided currently by the test measuring telomere length is to obtain different serial measurements (relative to the number and percentage of critically short telomeres and their wear rate) within an annual health assessment program. In this way, the doctor can obtain more information about the patient, helping them determine what actions they should take to improve their situation.
There are different techniques to measure telomeres. For example, the technique known as PCR (Polymerase Chain Reaction) consisting of an amplification signal of single copy genes. It is a simple method by which a report is generated that, using a graph shows the average telomere length; however, this graph ignores critically short telomeres, so it is a very precise technique.
Flow Fish is another system used to analyze the length of telomeres in a cell population after hybridization with a fluorescent probe. The methodology is more quantitative and reproducible than the previous case. Nevertheless, it does not present personalized information on telomeres, or on critically short telomeres.
Only the TAT® (Telomere Analysis Technology) technique makes it possible to determine the length of telomeres at the individual level, of both cell and tissue samples, making it possible to quantify the abundance of critically short telomeres. Consequently, providing an estimate of the biological age of each person is achieved using the percentage of excessively short telomeres measured in blood as an indicator for the overall body as a basis.
TAT results provide medical information of great scientific value, which will not only have a preventive nature but will help the doctor in treating the evolution of different pathologies. It is therefore about improving the quality of information on each patient, with the ambitious goals of improving both their life expectancy, as well as their quality of life. We don’t know for sure whether we will manage to achieve immortality someday. What we do know is that we are increasingly closer to living longer and better. All thanks to the information provided to us by telomere measurement.
Stephen J. Matlin
References:
[1] Müller HJ. The remaking of chromosomes. Collecting Net 1938; 13:181-198; McClintock B. The stability of broken ends of chromosomes in Zea mays. Genetics 1941; 26: 234-282
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