Nicotinamide adenine dinucleotide (NAD+): essential redox metabolite, co-substrate and an anti-cancer and anti-ageing therapeutic target.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic and preclinical research without systematic methodology or new human data.
PubMed 32573651 · doi:10.1042/BST20190033
What was done
This narrative review summarizes the biological roles of nicotinamide adenine dinucleotide (NAD+) and NADH in redox metabolism and as catalytic co-substrates for enzymes including sirtuins and PARPs. It reviews NAD+ homeostasis, the age-related decline of NAD+ in tissues, dietary supplementation with NAD+ precursors, cancer dependency on NAD+, therapeutic targeting of NAMPT in the tumor microenvironment, and techniques for measuring subcellular NAD+ dynamics.
What was found
The abstract reports no quantitative values or statistical effect sizes. It qualitatively describes that NAD+ concentrations decrease with age in the human brain and peripheral organs, correlating with neurodegeneration, while many malignancies show heightened dependency on NAD+ metabolism. The author notes that clinical attempts to therapeutically exploit NAD+ metabolism in cancer have achieved limited success so far.
Why it matters
It highlights the contrasting therapeutic opportunities in NAD+ biology: elevating NAD+ pools to mitigate age-related diseases versus disrupting NAD+ synthesis pathways to inhibit tumor metabolism.
Limits
As a narrative review, it presents mechanistic syntheses rather than systematic review metrics or new empirical clinical trials. No sample sizes, effect estimates, or formal risk-of-bias evaluations are reported in the abstract.
Cited by
- supports Sirtuins require NAD as a cofactor/fuel to regulate gene expression and repair broken DNA.