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Have you ever wished for a miracle cure to slow the aging process?

The ends of chromosomes are protected by specific DNA sequences called telomeres, visualized here in red. Image by Thomas Ried, Center for Cancer Research, National Cancer Institute

Role of Telomeres

Our genes are twisted double-stranded DNA molecules called chromosomes. Telomeres are DNA lengths found at the ends of chromosomes that maintain our genetic info, allow cells to divide, and contain some secrets on how we age and get cancer.
Like the plastic tips on shoelaces, telomeres prevent fraying and adhering, which would otherwise destroy or scramble an organism’s genetic information.
But as cells divide, their telomeres shrink. The cell becomes dormant, “senescent,” or dies if they are too short. This shortening process is linked to age, cancer, and mortality

Why Chromosomes need Telomeres?

Telomeres enable cells to divide while retaining all of their genes. Cell division is required to form new skin, blood, bone, and other types of cells.
Without telomeres, chromosome ends may merge and alter the genetic design of the cell, resulting in malfunction, cancer, or cell death. Without telomeres, chromosome ends would appear to have damaged DNA, and the cell would attempt to repair something that was not broken, which would also cause them to cease division and eventually perish.

What happens when a cell divides?

Before a cell divides, it duplicates its chromosomes to ensure that both resultant cells have the same genetic material. To be copied, the two DNA strands of a chromosome must unwind and separate. After that, an enzyme (DNA polymerase) reads the existing strands and constructs two new ones. It initiates the process with the assistance of tiny strands of RNA. Each new matched strand is slightly shorter than the original strand upon completion due to the space required at the end for this little piece of RNA.

Who is Telomerase?

Telomerase, an enzyme, adds nucleotides to the ends of telomeres. Telomerase prevents telomeres from wearing down excessively in young cells. However, as cells divide frequently, there is insufficient telomerase, and the telomeres shorten, resulting in cell aging.
Telomerase is still active in sperm and eggs, which are passed down through generations. Without telomerase to maintain the length of their telomeres, every organism with reproductive cells would quickly become extinct.

Telomeres in cancer study

When a cell becomes cancerous, it divides more frequently, and its telomeres become extremely short. If a cell’s telomeres become too short, it may die. These cells often evade death by producing additional telomerase enzyme, which prevents the telomeres from shortening further.

Telomerase measurement may be used to detect cancer. Researchers inhibited telomerase activity in laboratory-grown human breast and prostate cancer cells in one experiment, causing the tumor cells to die. However, there are risks. One may impair fertility, wound healing, and blood and immune system cell production by inhibiting telomerase. Furthermore, if scientists can figure out how to inhibit telomerase, they may combat cancer by causing cancer cells to age and die.

Telomeres in the aging process

While telomere shortening has been linked to the aging process, it is unknown whether shorter telomeres are merely a sign of aging, similar to gray hair, or whether they cause aging.
If telomerase governs immortality in cancer cells, could it also prevent normal cells from aging? Could telomerase be used to prolong life by preserving or restoring the length of telomeres? If this is the case, does this increase our risk of contracting cancer?
Scientists are unsure at the moment. However, they have used telomerase in the laboratory to keep human cells dividing far beyond their normal limit while avoiding cancer.
Suppose we used telomerase to “immortalize” human cells. In that case, we might be able to mass-produce cells for transplantation, such as insulin-producing cells for diabetes treatment, muscle cells for muscular dystrophy treatment, cartilage cells for certain types of arthritis treatment, and skin cells for severe burns and wound healing. A seemingly endless supply of normal human cells grown in the laboratory would also aid in testing new drugs and gene therapies.

What the future holds for human longevity

By measuring telomere length in the blood, “what you are reporting on is the capacity of immune stem cells to function normally,” explained Matt Kaeberlein, a University of Washington researcher. He studies the molecular basis of aging. “What this could mean is that the immune system is especially susceptible to lifestyle and environmental factors.”

According to researchers Miguel A. Muoz-Lorente, Alba C. Cano-Martin, and Maria A. Blasco, mice with longer telomeres showed minor DNA damage as they age. The mice with hyper-long telomeres are lean, have low cholesterol and LDL levels, and have improved glucose and insulin tolerance. Additionally, mice with hyper-long telomeres have a lower cancer incidence and a longer lifespan. These findings demonstrate that having telomeres longer than average in a given species does not have a harmful effect but instead has a beneficial impact.

Elissa S. Epel, Elizabeth H. Blackburn, Jue Lin, and Firdaus S. Dhabhar demonstrate that psychological stress—both perceived stress and chronic stress—is significantly associated with increased oxidative stress, decreased telomerase activity, and shorter telomere length in peripheral blood mononuclear cells from healthy patients. Women who report high levels of perceived stress have telomeres that are on average shorter by the equivalent of at least one decade of additional aging than women who report low levels of perceived stress. These findings have implications for our understanding of how stress may contribute to the earlier onset of age-related diseases at the cellular level.
According to Cawthon, if all aging processes could be halted and oxidative stress damage repaired, “one estimate is that people could live 1,000 years.”



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Muñoz-Lorente, Miguel A., et al. “Mice with Hyper-Long Telomeres Show Less Metabolic Aging and Longer Lifespans.” Nature Communications, vol. 10, no. 1, 2019,