Studies using worm and mouse models of a neurodegenerative disease indicate that the coenzyme NAD+ can help extend life and postpone aging processes by facilitating DNA repair and the culling of poorly functioning mitochondria. [Image courtesy of University of Copenhagen The Faculty of Health and Medical Sciences]
Studies using worm and mouse models of a neurodegenerative disease indicate that the coenzyme NAD+ can help extend life and postpone aging processes by facilitating DNA repair and the culling of poorly functioning mitochondria. [Image courtesy of University of Copenhagen The Faculty of Health and Medical Sciences]

It’s a coenzyme that occurs in all living cells, it’s necessary for carrying out metabolically significant redox reactions, and it’s known to play a role in aging processes. It is nicotinamide adenine dinucleotide (NAD). When the oxidized form of this substance, NAD+, is added to animal models, it appears to extend life and postpone the onset of the aging process. Yet the mechanisms behind these effects have remained unclear, limiting the degree to which NAD+ may be exploited for therapeutic purposes.

In hopes of clearing up the uncertainty surrounding NAD+ mechanisms, an international team of scientists from the University of Copenhagen and the National Institutes of Health (NIH) decided to investigate how NAD+ works in animal models of ataxia telangiectasia (A-T), a genetic disease characterized by progressive neurodegeneration and the gradual loss of coordination via cerebellar atrophy. The team found that NAD+ bridges the gap between two aging mechanisms: less effective DNA repair and less effective culling of defective mitochondria.

Details of the work appeared October 11 in the journal Cell Metabolism, in an article entitled, “NAD+ Replenishment Improves Lifespan and Healthspan in Ataxia Telangiectasia Models via Mitophagy and DNA Repair.” The article asserts that replenishing intracellular NAD+ in mouse and roundworm models can reduce the severity of A-T neuropathology, normalize neuromuscular function, delay memory loss, and extend lifespan.

“Mechanistically, treatments that increase intracellular NAD+ stimulate neuronal DNA repair and improve mitochondrial quality via mitophagy,” the article’s authors explained. “This work links two major theories on aging, DNA damage accumulation and mitochondrial dysfunction through nuclear DNA damage-induced nuclear-mitochondrial signaling, and demonstrates that they are important pathophysiological determinants in premature aging of A-T, pointing to therapeutic interventions.”

“Our new study shows an age-dependent decrease in the level of NAD+, and this decrease is far greater for organisms with early aging and a lack of DNA repairs,” noted Professor Vilhelm Bohr from the Center for Healthy Aging and the National Institute of Health. “We were surprised to see that adding NAD+ postponed both the aging processes of the cells and extended life in worms and in a mouse model.”

Even though the researchers have only examined the effect of the substance on model organisms and have not administered the substance to patients, they expect to see the same effect in humans, as the cell repair mechanisms are universal for the cells of all living organisms. Understanding the universal mechanisms at the cellular level is key to understanding human aging and why we become more susceptible to illness as we grow older. Hopefully, this new knowledge will be able to help postpone physical aging processes and prevent illnesses such as Alzheimer's and Parkinson's diseases.








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