What are telomeres?
Telomeres are structures consisting of self-repeating DNA sequences and associated proteins that do not encode any genes. They protect the ends of chromosomes (the genetic units formed by the condensation of DNA with the help of proteins and which provide heredity in living organisms) against degradation.
How does it work?
During cell division, DNA is replicated and this is called DNA replication. Due to the nature of DNA replication during replication, the very end of the chromosome cannot be copied. Telomeres, which are repetitive sequences located at the very end of the chromosome, prevent the natural ends of the DNA from mixing with damaged DNA. So, we can think of telomeres as protective caps. Therefore, telomeres naturally shorten with each cell division. This shortening acts as a kind of “biological clock” that counts down to a point where the cell can no longer divide. But is it possible to stop telomeres from shortening?
The shocking link between cancer and longevity: Telomerase
The enzyme (reaction accelerator biomolecule) called telomerase is composed of both RNA and protein components. The RNA component acts as a template, like a carbon copy paper, allowing new DNA sequences to be added to the ends of chromosomes. This prevents the DNA from becoming too short during each cell division.
Telomerase plays a key role in maintaining the length of telomeres, especially in cells that divide frequently, such as stem cells and some immune cells. Unfortunately, telomerase is also reactivated in many cancer cells. This allows cancer cells to divide continuously without undergoing the normal cell death (apoptosis) process associated with aging.
Implications for treatment
The understanding of the role of telomerase in the maintenance of telomere length has led to the search for therapeutic strategies.
Inhibition of telomerase is considered a potential strategy for cancer treatment as it may limit the ability of cancer cells to proliferate.
In contrast, in the field of aging research, approaches to increase telomerase activity as a means to counteract age-related telomere shortening and promote healthy cell function are beginning to be applied.
Long Telomeres – Long life?
Throughout human life, telomeres naturally shorten with each cell division. Over time, this shortening contributes to cellular aging (senescence) and eventually reaches a point where cells lose their ability to divide.
Shortened telomeres are associated with several age-related diseases, including cardiovascular diseases, neurodegenerative disorders (the process by which nerve cells deteriorate and die over time) and some cancers. The link between telomere length and age-related shortening has led to research into whether preserving telomere length can influence the aging process.
Research in model organisms such as mice has shown that preserving telomere length through activated telomerase can delay age-related pathologies and prolong life span. However, transferring these findings to humans requires a much more complex experimental setup and process, while the role of telomerase in human longevity is still under investigation.
Considerations and Challenges
Efforts to increase telomerase activity include the challenge of preventing uncontrolled cell division while promoting healthy cellular function. A nuanced understanding of how telomerase effects on longevity affects different cell populations is crucial for developing targeted interventions.
In conclusion, while there is evidence to suggest that preservation of telomere length may have positive effects on aging, due to the cancer risk that may result from more than tolerable telomerase activity, further research is important before practical applications in humans.
References:
Shin JS, Hong A, Solomon MJ, Lee CS. The role of telomeres and telomerase in the pathology of human cancer and aging. Pathology. 2006 Apr;38(2):103-13. doi: 10.1080/00313020600580468. PMID: 16581649.
Lulkiewicz M, Bajsert J, Kopczynski P, Barczak W, Rubis B. Telomere length: how the length makes a difference. Mol Biol Rep. 2020 Sep;47(9):7181-7188. doi: 10.1007/s11033-020-05551-y. Epub 2020 Sep 2. PMID: 32876842; PMCID: PMC7561533.
Shawi M, Autexier C. Telomerase, senescence and ageing. Mech Ageing Dev. 2008 Jan-Feb;129(1-2):3-10. doi: 10.1016/j.mad.2007.11.007. Epub 2007 Dec 14. PMID: 18215413.
