期刊
AGING AND DISEASE
卷 12, 期 8, 页码 1879-1897出版社
INT SOC AGING & DISEASE
DOI: 10.14336/AD.2021.0523
关键词
NAD(+); NA; NAM; NMN; NR; aging
资金
- Natural Science Foundation of China [81730092, 81973315]
- Jiangsu Key Laboratory of Neuropsychiatric Diseases [BM201 3003]
- Priority Academic Program Development of the Jiangsu Higher Education Institutes (PAPD)
Coenzyme I (NAD(+)/NADH) and coenzyme II (NADP(+)/NADPH) play important roles in biological processes, with NAD(+) synthesized through de novo and salvage pathways and NADH levels increasing in aged brain tissue. The ratio of NAD+/NADH affects cellular metabolism, ATP production, and other functions.
Coenzyme I (nicotinamide adenine dinucleotide, NAD(+)/NADH) and coenzyme II (nicotinamide adenine dinucleotide phosphate, NADP(+)/NADPH) are involved in various biological processes in mammalian cells. NAD(+) is synthesised through the de novo and salvage pathways, whereas coenzyme II cannot be synthesised de novo. NAD(+) is a precursor of coenzyme II. Although NAD(+) is synthesised in sufficient amounts under normal conditions, shortage in its supply due to over consumption and its decreased synthesis has been observed with increasing age and under certain disease conditions. Several studies have proved that in a wide range of tissues, such as liver, skin, muscle, pancreas, and fat, the level of NAD(+) decreases with age. However, in the brain tissue, the level of NADH gradually increases and that of NAD(+) decreases in aged people. The ratio of NAD+/NADH indicates the cellular redox state. A decrease in this ratio affects the cellular anaerobic glycolysis and oxidative phosphorylation functions, which reduces the ability of cells to produce ATP. Therefore, increasing the exogenous NAD(+) supply under certain disease conditions or in elderly people may be beneficial. Precursors of NAD(+) have been extensively explored and have been reported to effectively increase NAD(+) levels and possess a broad range of functions. In this review article, we discuss the pharmacokinetics and pharmacodynamics of NAD(+) precursors.
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