IS NAD+ THE FUTURE OF ANTI-AGING?

Key Pointers

NAD+ is an important cofactor in biological systems as it is involved in the following reactions:

  • NAD+ is involved in all fundamental biological processes.
  • NAD+ is anti-aging and anti-inflammatory as it improves the functions of important organelles such as mitochondria.
  • NAD+ is involved in energy production, gene expression, DNA repair, and oxidative stress.

Before we discuss the future of NAD+ as anti-aging, we have to understand what aging is. Aging is the deterioration of vital organelles, so the cell is being distorted due to a lack of energy production. The vital nutrients are not able to be utilised and aging occurs. 


There are four stages of aging:


  • Self-sufficiency - Where the person prefers being independent and is self-reliant.
  • Interdependence - The person becomes more reliant on others for assistance.
  • Dependency - At this stage, the person's physiological functioning declines.
  • The fourth stage is infirmity 
  • Fifth is the end of life.

Recent studies and research show that the aging process can be reversed or aging symptoms can be delayed by using different cofactors and drugs. These cofactors or drugs are either inhibitors of some enzymes or stimulators of some enzymes. Nicotinamide adenine dinucleotide (NAD+) works as cofactors for many enzymes and also transducers of certain genes, such as 78c.


By increasing the level of NAD+, 78c is induced for protein production which ameliorates metabolic or other disruptions involved in aging.


NAD+ is involved in gene expression, DNA repair, oxidative stress, and energy production. All these factors help in delaying or reverse the aging process. 


How NAD is Anti-aging? 


Sirtuins is a hormone used to increase the lifespan of the cell. Sirtuins are evolutionarily conserved NAD-dependent deacetylases. It is shown that NAD+-SIRT1 signaling promotes the mitochondrial process.


Another method is PARPs are expressed by my eukaryotic cell involved in DNA damage detection, repair, and cell death pathway. Overactivation of PARP 1 leads to depletion of NAD+, and cell death occurs as mitochondrial function is lost and aging occurs. But the increased number of NAD+ when SIRT1 is intact can reduce cell death through activation of PARP1. CD38 causes an imbalance of NAD+ and reduced NADH which leads to cell death and the aging process.

 

NAD+ is an inducer of a gene that helps in the production of a protein called 78C. This 78c protein stops the action of another protein CD38. CD38 causes aging through a different mechanism. So by producing protein 78C, NAD+ acts as an anti-aging molecule. NAD+ inhibitors enzymes are involved in aging as these depleted NAD+ levels. No DNA repair, no energy, no gene expression, and the aging process going on. CD38 , PARP and SARM1 all degrade NAD+.

The measure of the anti-aging ability of NAD+ is through RNA sequence. All the factors with which NAD+ deals are essential for the improvement in the aging process. Because information due to oxidative stress, DNA damage, gene suppression leads to the negative aging process.

CONCLUSION

NAD+ is an important cofactor involved in anti-aging as it synthesis sirtuins enzymes. NAD+ acts as anti-aging as an activator of PARP1 and also acts as an inhibitor of CD38. Due to all these reactions, it lifts the deteriorating cells due to senile changes and protects us from different age-related diseases. The higher level of NAD+ increases the life span of the cell.

REFERENCES

  • Taosheng Huang, The Role of NAD+ in Anti-Aging Therapies. Am J Biomed Sci & Res. 2019 - 6(5). AJBSR.MS.ID.001080. DOI: 10.34297/AJBSR.2019.06.001080 
  • Zhavoronkov A, et al. Classifying aging as a disease in the context of ICD-11. Front Genet. 2015. November 4;6:326. 
  • Schultz MB, et al. Why NAD+ Declines during Aging: It’s Destroyed. Cell Metab. 2016. June 14; 23(6): 965–966 
  • Zhu XH, et al. In vivo NAD assay reveals the intracellular NAD contents and redox state in the healthy human brain and their age dependences. Proc. Natl. Acad. Sci. 2015; 112:2876–2881