According to Leonard Hayflick, typical human cells are mortal and have a limit to the much they can replicate, and the older cells often reach the replication limit earlier than younger cells. The Hayflick limit has a direct correlation to the number of DNA repeats that are found at the end of chromosomes that are bearing of genetic material. The repeats of the DNA are part of the larger process of protecting capping structures, which are called telomeres, which are responsible for safeguarding the ends of chromosomes from rearrangements of the DNA that can result in possible destabilization of the genome. Telomerase is the unique key that reverses the aging process. With each division of the telomeric DNA, there is an increase in the eventual failure of securing the ends of the chromosomes and this replicates the actions of a molecular clock ticking towards the end of a cell growing. This is often associated with the process of aging and resultant conditions such as organ failure, sicknesses, inability to carry out tasks normally and wrinkling (de Oliveira Junior 2015).
Research
Professor Julian Chen carried out a laboratory research from the Arizona State University in the School of Molecular Sciences to come up with the conclusions that helped in uncovering a step that was crucial to the catalytic cycle of the telomerase enzyme. This catalytic cycle is determinant of the ability for DNA repeats to be synthesized by telomerase enzymes onto chromosome ends thus resulting in immortality of cells. This new perspective offers an effective and new avenue to understand therapeutics that relate to anti-aging research. Through developing a system to counteract the shrinking process of telomere will result in an extension in the lifespan of a cell, therefore, the lifespan of an individual.
Gradual shrinking of telomeres has a resultant negative effect on the capacity of replication of human adult stem cells, which perform the functions of restoration of and replenishment of aging organs and damaged tissues. Slowing down the activity of telomerase in an adult’s stem cells does not result in immortality; however, there is a go slow in the molecular clock. In aged adults, the telomere length being shortened is the factor that results in difficulties in healing resulting in longer healing periods and increased degradation of tissue that limits bodily functions (Humphreys et al. 2016).
In developing an understanding of the telomerase enzyme, how to regulate and limit its functioning gives a promise of ability to reverse the shortening cycle and cellular aging with increased potential for improving the well-being and overall health of individuals who are elderly while possibly increasing the lifespan of adults. The professor said that the recent discovery made was an important medical discovery that relates to limitation of DNA repeats to help increase lifespan (Jafri 2016).
Discussion
The telomerase enzyme has an intrinsic brake which is coded within the telomerase, and this is what the enzyme uses to control DNA synthesis. The intrinsic brake works within each replenishment cycle of a DNA sequencing repeat. Telomerase activity is negatively affected by human diseases such as idiopathic pulmonary fibrosis, dyskeratosis congenita and aplastic anemia which are linked to mutation and they also result in the loss of the length of telomere. The acceleration in the shortening process is similar to premature aging that shortens the lifespan of a patient and leads to an increase in the deterioration of an organ. The treatment of these diseases is achievable through an increase in activity of telomerase (de Oliveira Junior 2015).
However, despite telomerase cells having an effect of curing diseases that cause premature aging and giving youth to prematurely aging cells, an excess of the enzyme can prove harmful to the individual. Youthful stem cells make use of telomerase to offset length loss of telomere and similarly, cancerous cells make use of telomerase for purposes of maintenance of the destructive growth. There is need for precision in augmentation and regulation of the functioning of telomerase with a balance being created between cell rejuvenation and increasing chances of cancerous cells developing (Anna et al. 2017).
Somatic cells, which are distinct from human stem cells, comprise of the majority cells found inside the human body and have no telomerase activity. These reduce development of cancerous skills due to lack of telomerase activity. It is important for drugs that reduce the activity of telomerase in human cells to reduce chances for development of cancerous cells. This discovery is a new target for drug manufacturers where the new drugs can augment the activity of telomerase. Also, anti-aging therapies can be developed to target specific stem cells without posing a risk of cancer development with an increase in telomerase activity (de Oliveira Junior 2015).
References
Anna, Meiliana, et al. "Telomeres and Telomerase in the Aging Heart." Indonesian Biomedical Journal, Vol 9, Iss 3, Pp 129-42 (2017), no. 3, 2017, p. 129. EBSCOhost, doi:10.18585/inabj.v9i3.389.
de Oliveira Junior, Robson Jose. "Telomerase and Cancer Research." Biochemistry " Molecular Biology Journal 1.1 (2015).
Humphreys, K. L., Esteves, K., Zeanah, C. H., Fox, N. A., Nelson, C. A., " Drury, S. S. (2016). Accelerated telomere shortening: Tracking the lasting impact of early institutional care at the cellular level. Psychiatry research, 246, 95-100.
Jafri, Mohammad A., et al. "Roles of telomeres and telomerase in cancer, and advances in telomerase-targeted therapies." Genome medicine 8.1 (2016): 69.
