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Role of Telomerase Reactivation in Slowing Senescence Term Paper


Ageing is considered as a process of extreme complexity that affects not only the individual cells, but also the body as a whole. This research thesis will hence focus on the effect of telomeres, organismal aging, as well as how telomere maintenance affects the genome stability.

The telomere is a fraction of the complex process involved in ageing hence this research will elaborate how DNA damage response and genome integrity influence postmitotic ageing. In addition to this, the genetic pathways that enhance the elongation of life and survival will also be elaborated.


In the modern world, the ageing population has become a topic of interest. The curiosity in this field has led to researches in terms of regenerative remedies where scientists tend to investigate whether there is a possibility of doing away with intrinsic instigators for the sole purpose of reversing, if not halting, the degeneration that brings about ageing.

There is accumulation of evidence over the years that indicate telomere damage as a key factor in bringing about decline in organs and disease risks that are associated with ageing. In humans, evidence obtained also indicated strong links between reduction of telomeres, high risk of attaining diseases associated with ageing and failure of organ system in terms of degenerative diseases[1].

According to Rudolph, ageing is has a huge impact on the lifestyle, disease prevention and patient’s care of individuals throughout the world. Main mechanisms of molecules that have an impact on ageing process are 1) reduction in the stem cell function of adults; 2) Alteration in metabolic pathways and gene expressions; and 3) increase in molecular damage thereby affecting the proteins and DNA[2].


The alternative hypothesis in this research is that “telomerase reactivation slows down senescence” while on the other hand, the null hypothesis in this research is any other outcome of the research undertaken.

Upon conducting an experiment on an adult mouse to establish the effects of physiological telomerase activated throughout the organ systems and cell types, it was established that the G4TERT-ER mice possessed high degenerative phenotypes. In addition, the telomerase reactivation generated a restitution of the telomere reserves, while there was observation of suppressed DNA damage signaling and enhanced organ system with light cellular checkpoint responses.

This experiment hence gives rise to speculation of tissue stem cells being retained in an intact quiescent form while at the same time they can perform normal repopulation function if the genotoxic stress at telomeres is eliminated. Carcinogenesis was not promoted in this experiment despite the instability in chromos caused by insufficient telomeres reactivation. In spite of this, there is a possibility that more reactivation of prolonged telomerase may lead to Carcinogenesis.

In addition to this, it was noted that the effects of age-associated in the brain functions of mammals are linked to “accumulation of DNA damage and the continuous reduction in myelination and neurogenesis”[3]. On the data attained, it was established that telomere dysfunction together with telomerase reactivation in the mice had the ability to restore SVZ neurogenesis.

The results attained on conclusion of the test were relatively consistent with the test results previously conducted that portrayed the negative effects upon detecting the odor thresholds that resulted from extensive inhibition of neurogenesis in SVZ.

In summation, when vital organs of the body together with the central nervous system decline due to age-related factors, then this will mean evidence of telomere rejuvenation as means of diseases that are age related especially the diseases are driven by the accumulation of genotoxic stress[4].

According to Andrews and Tollefsbol, telomerase is normally in form of embryonic and germline as well as somatic stem cell although in this case they are hardly detectable in most of adult’s somatic cells. Replicative senescence is induced by actively division of somatic cells that results to shortening of telomeres with concurrently with each cell replication. In addition, this phenomenon has given rise to the notion that reduction in terms of expression of telomerase in somatic cells may trigger in motion an ageing process molecular clock[5].

Telomerase reactivation is essential particularly on proliferative organs thus making it a marked impact. On brain health, the benefits are major determinants of declining health due to progressive age. As brain in mammals’ ages, the brain tends to indicate the accumulating DNA damage. In addition to this, the neurogenesis is restricted progressively as re-myelination is impaired all because of a declined neural stem and progenitor cell proliferation[6].

The primary role played by mRNA is translation in the extension of life span or reduction of TOR signaling. In addition to this life span is increased by ribosomal proteins, translation of initiation factors and undertaking of ribosomal S6 kinase mutations[7]

According to Mariela Jaskelioff, by accelerating DNA repair is essential in reversing DNA damage, which is a common stimulus of the senescent pathways. Before the use of designer drugs, the balance between excessive proliferation and senescence must be considered carefully. In addition, extensive research on the nexus between damage and DNA transcription will aid in identifying targets that particularly link ageing phenotypes[8].

The information on attained from aging studies plays a major role in identifying and specifying cellular dysfunction that lead to various degenerative diseases. Further studies on stem cell science are also important in while dealing with approaches pertaining to ageing dysfunction[9].

According to the cellular theory, the human aging can be attributed to cellular ageing. An explanation of the mechanisms undertaken on measurement of cell division and in determination of the appropriate cessation of replication is indicated by the telomere theory. Cell senescence signaling is cited as a signal when telomeres shorten to a length that is limited. Evidence of ramification of cellular senescence is indicated by age-associated cardiovascular disease[10].

Telomerase enzyme plays a great role in senescence process. Chromosomes are protected by telomeres, which is one of their functions. The chromosomes are normally shortened after each cell division thus the shorter the telomerase the older the cell. The telomerase enzyme normally restores the telomeres to its original size after cell division. This means the chromosomal caps will hence remain intact thus giving the stem cells an eternal life. [11]

Reduced levels of cellular senescence is suggested to be the as the main effect of having caloric restriction. This outcome may result from the signaling suppression of S6K1 and mTOR[12].

Impact of on evolution- Darwinian medicine

The human lifespan of evolution have been cut short by a number of factors. Some of these factors include; malnutrition, infectious diseases and accidents. Despite the traits being deleterious, in evolution, genes that influence fertility and survival are the ones that are selected. Recent evolution theories term ageing as together with its biological correlates as unpredicted aftermath of selection that are strong in early life operation than the life after[13].

In humans, the antioxidant defenses are used to remove the reactive oxygen species produced in the vivo although not all of it is removed. A few remain only to cause damage. Primarily, the main evidence of damage is usually witnessed in DNA where there the reaction is seen to cause mutagenic abrasion, leading to it being relatively dysfunctional.

According to evidence attained, there is use in free-radical production; “the white blood cells at inflammation sites release reactive oxygen species that is normally used in killing fungi and bacteria”[14] as well as inactivating viruses. The natural selection would hence pick this important defense as the “preferable in evolution, as it will be essential in the prevention of early death due to infection”[15].

According to Crews, the multiple phenotypic variations of humans are structured quantitatively by influences of evolutionary forces that develop genetic influences. This genetic variability influences the life history of humans and the evolutionary forces have a detailed human life span and senescence. As mutation occurs, the DNA of organisms alters continually[16].

The Darwinian concept of fitness as a foundation of natural selection relies mainly on the relative net reproduction output of people within a population who are considered to be competing for resources that are limited. In this theory, questions on lifespan reproductive capacity are confronted. This will hence represent a value of the summation of reproduction throughout the existing population from maturity of individuals to reproductive senescence.

The main parameters are normally the number of offspring produced over the different ages, their developmental abnormalities, and their viability. Conclusively, genetics models in population dictate that natural selection normally acts to increase the intrinsic rate in a population[17].

According to Nomura, Takeda and Okuma, throughout a lifespan, aging is regulated by environmental and genetic factors in a multi-factorial manner. The effects of the different environmental factors on phenotype are hence clarified for the sole purpose of gaining a clear understanding of the aging process. These environmental factors include; nutritional status, various kinds of exogenous stress on phenotypes and microbiological condition[18].


Despite the researches conducted on telomerase indicating that there may be presence of telomerase in senescent cells, the notion of having this enzyme present alone is not enough to avoid cellular senescence. According to the information gathered from aging studies cellular dysfunction is specified and identified as a cause to numerous generative diseases. In addition to this research on stem cell science is crucial especially when dealing with strategies that incorporate ageing dysfunction.

The enzyme telomerase has a major role to play in the senescence process. It is considered as an important target while dealing with increase in cellular life span. However many questions pertaining to the mechanism of cellular senescence remain a mystery. This dilemma arises mainly when considering the correlation between human senescence and cellular senescence. The answers to these unanswered questions may lead to the strategy of slowing down the biological clock.


Andrews, Lucy & Tollefsbol, Trygve. . NJ: Humana Press Inc., 2007. Web.

Couteur, David Le and Simpson, Stephen. Adaptive senectitude: The Prolongevity Effects of Aging. Sydney: Oxford University Press, 2010. Web.

Crews, Douglas. . London: The Press syndicate of The University of Cambridge, 2003. Web.

Finch, Caleb E. . London: The University of Chicago Press, Ltd, 1990. Web.

Halliwell, Barry. Ageing and Disease: From Darwinian Medicine to Antioxidants? World Scientific Publishing Company, 2004. Web.

Jaskelioff, Mariela et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. New Delhi: Macmillan Publishers Limited, 2010.

Kirkland, James. : NY: Published online, 2010. Web.

Loue, Sana & Sajatovic, Martha. Encyclopedia of Aging and Public Health. Ohio: Springer Science+Business Media, LLC, 2008. Web.

Marin-Garcia, Jose. . NJ: Springer Science+Business Media, LLC. 2008. Web.

Mummery, Christine et al. . MA: Elsevier Inc, 2011. Web.

Nomura, Yasuyuki et al. The senescence-accelerated mouse (SAM): an animal model of senescence. Amsterdam: Elsevier B. V., 2004. Web.

Rudolph, Lenhard. : molecular mechanisms. Berlin: Springer-Verlag Berlin Heidelberg, 2008. Web.

Seymour, Robert and Doncaster, Patrick. : London: Published online, 2007. Web.

Tavernarakis, Nektarios. Protein Metabolism and Homeostasis in Aging. NY: Landes Bioscience and Springer Science+Business Media, LLC, 2010. Web.

Vergel, Mar et al. , 2010. Web.


  1. Mariela Jaskelioff, et al, Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice, (New Delhi, Macmillan Publishers Limited, 2010), p. 1.
  2. Lenhard Rudolph, Telomeres and telomerase in aging, disease, and cancer: molecular mechanisms, (Berlin, Springer-Verlag Berlin Heidelberg, 2008), p.xi
  3. Mariela Jaskelioff, et al, ibid.
  4. Mariela Jaskelioff, et al, ibid, p. 5
  5. Lucy Andrews & Trygve Tollefsbol, Telomerase inhibition: strategies and protocols, (NJ, Humana Press Inc., 2007), p.2
  6. Mariela Jaskelioff, et al, ibid, p. 2
  7. Nektarios Tavernarakis, Protein Metabolism and Homeostasis in Aging. (Texas, Landes Bioscience and Springer Science+Business Media, LLC, 2010) p.20
  8. Mar Vergel, et al, Cellular Senescence as a Target in Cancer Control, (Published online, 2010), par. 10
  9. Jose Marin-Garcia., Aging and the heart: a post-genomic view, (NJ, Springer Science+Business Media, LLC. 2008) p. 524
  10. Sana Loue & Martha Sajatovic, Encyclopedia of Aging and Public Health, (Ohio, Springer Science+Business Media, LLC, 2008), P. 199
  11. Christine Mummery, et al, Stem Cells: Scientific Facts and Fiction, (MA, Elsevier Inc, 2011), P. 51
  12. James L. Kirkland, Perspectives on cellular senescence and short term dietary restriction in adults, (NY, Published online, 2010)
  13. David G. Le Couteur and Stephen J. Simpson, Adaptive senectitude: The Prolongevity Effects of Aging (Sydney, Oxford University Press, 2010) par 11
  14. Barry Halliwell, Ageing and Disease: From Darwinian Medicine to Antioxidants? (World Scientific Publishing Company, 2004), p. 4 & 5.
  15. Barry Halliwell, Ageing and Disease: From Darwinian Medicine to Antioxidants? (World Scientific Publishing Company, 2004), p. 4 & 5.
  16. Douglas Crews, Human senescence: evolutionary and biocultural perspectives, (London, The Press syndicate of The University of Cambridge, 2003), P. 11
  17. Robert M Seymour and C. Patrick Doncaster, Density Dependence Triggers Runaway Selection of Reduced Senescence, (London, Published online, 2007) p. 3
  18. Yasuyuki Nomura, et al, The senescence-accelerated mouse (SAM): an animal model of senescence, (Amsterdam, Elsevier B. V, 2004), p. 3 & 4.
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IvyPanda. "Role of Telomerase Reactivation in Slowing Senescence." May 14, 2020.


IvyPanda. 2020. "Role of Telomerase Reactivation in Slowing Senescence." May 14, 2020.


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