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Telomeres and NAD+

An image showing telomeres and DNA

Cell proliferation is essential for the survival of all complex creatures. Cells must reproduce in order to maintain growth and restore cells that have been killed. There is, however, a defect in this method of operation. It is usual for errors to be made in the replication of DNA strands at the ends of the strands because of the inherent flaws in DNA replication.

Typically, the ends of DNA strands are lost, which can be a source of worry since genes located at the ends of the DNA strands may be shortened as a result. Fortunately, each chromosome has a unique replicative DNA sequence known as Telomeres, which are found only on one copy of each chromosome. Despite the fact that telomeres shrink with each replication, an enzyme known as telomerase may be able to repair them. The telomere also preserves the end of a chromosome by preventing it from being misunderstood as a DNA double-strand break. This prevents the chromosomes from being ligated together by DNA repair machinery, a behavior that is frequently observed in cancer cells.

Telomeres Shortening With Aging

Telomerase insufficiency is connected with the early onset of disorders that result in the loss of the regeneration ability of many tissues in humans. Telomere shortening is also associated with autophagy, another aging characteristic, as well as with organismal aging.

Furthermore, systemic viral transduction of telomerase may be used to postpone normal physiological aging in adult wild-type mice without increasing cancer incidence. Research shows that activating telomerase can reverse aging. The rapid aging of telomerase-deficient mice, in particular, can be reversed by genetically reactivating telomerase in these elderly animals. Observational studies in humans have established a substantial link between short telomeres and mortality risks.

Telomere dysfunction decreases NAD+ levels and suppresses sirtuins activity

A recent study discovered that patients with dyskeratosis congenital, a disease caused by short telomeres, and telomerase knockout mice both have lower nicotinamide adenine dinucleotide (NAD) levels and an imbalance in the NAD metabolome, including increased CD38 NADase activity and decreased PARP and SIRT1 activity.

NAD+ Precursors Can Help Aging. 

  • Research proved that supplementation with NAD precursors restored NAD homeostasis, relieving telomere damage, poor mitochondrial biosynthesis and clearance, cell growth inhibition, and cellular senescence.
  • Additionally, the second research demonstrates that treatment of the NAD+ precursor nicotinamide mononucleotide (NMN) prolongs telomeres, reduces DNA damage, enhances mitochondrial activity, and functionally restores liver fibrosis.

This research has revealed that NAD dysregulation contributes to telomere dysfunction on an immediate and fundamental level and that sirtuins are downstream targets of dysfunctional telomeres, respectively. Increasing NAD levels may also aid in the stabilization of telomeres and the relief of telomere-dependent illnesses, according to some research.

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