In the previous disclosure webblog 11, information referring to the genetic processes of cell differentiation and dedifferentiation are related to the formation of specialized tissues.

In the current webblog 12 genetic processes of cellular aging will be treated and for this we will focus on telomeres and telomerase in cells of eukaryotes beings, but not in prokaryotes.

Telomeres are DNA structures at the ends of chromosomes in all cells while telomerase is an enzyme, present in embryonic cells, able to insert genetic material into the telomeres that they lose in every process of duplication. It is therefore genetic structures (telomeres) and instruments to repair (telomerase).

In embryonic germ cells a large number of cell divisions are produced, each division involves a duplication of genetic material and each doubling involves the physical division of genetic material and the subsequent formation of new DNA helixes.

In the course of these operations losses of genetic material are produced such as the shortening of the terminals (telomeres). During the embryonic stage, this damage is not terribly relevant because telomeres and telomerase can manage the reconstruction of the telomere by the addition of genetic material especially TTAGGG fragments that are lost in each division, as the enzyme telomerase is composed of a ribonucleic acid-protein complex with reverse transcriptase activity (thus producing DNA from an RNA sequence itself of telomerase).

However the production of telomerase is repressed by genetic programming in mature somatic cells after birth, resulting in lack of repair of telomeres and progressive shortening after each cell division.

From the moment of birth the number of divisions is limited by genetics, but varies among species of plants and animals, between individuals of the same species and between tissues from the same individual, it is estimated between 2000 and 2500 repetitions.

Throughout the series, these lesions accumulate in DNA of telomeres and other chromosomal regions, the erosion of telomeres avoid chromosome protective function, it becomes unstable producing irreversible defects that prevent the duplication of genetic material resulting in the death programmed cell death (apoptosis).

When the number of cells that reach this situation is significant, the tissue and therefore the organ ages, and the individual exhausts its life cycle, even in the absence of external diseases or parasitic infections in it.

There are exceptions to this general rule and are the tumor cells that when dedifferentiate are able to resume the production of telomerase specific to embryonic stages. This results in the repair of their telomeres and enter a phase of uncontrolled growth.

Because of these mechanisms the individual is affected by aging (limited number of cell reproduction) or tumors (uncontrolled growth of undifferentiated cells that do not age)