What about NAD+

Highlights:  “NAD+ and sirtuins in aging and disease,” Shin-ichiro Imai and Leonard Guarente, Trends in Cell Biology, 2014, Aug. 24(8): 464-471. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112140/  71 references

• NAD ⁺ plays a key role in regulating metabolism and circadian rhythm through sirtuins.
  
• NAD ⁺ becomes limiting during aging, affecting sirtuins’ activities.
  
• NAD ⁺ decline is likely to be due to a NAD ⁺ biosynthesis defect and increased depletion.
  
• Supplementing key NAD ⁺ intermediates can restore NAD ⁺ levels and ameliorate age-associated pathophysiologies.
  

Another article (print full text, free) to read at the fitness center.
“NAD AND THE AGING PROCESS: ROLE IN LIFE, DEATH AND EVERYTHING IN BETWEEN” Mol Cell Endocrinol. 2017 Nov 5; 455: 62–74.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5419884/

“NAD was discovered over a hundred years ago (Harden and Young, 1906), and now that it has achieved its status as a super-centenarian molecule, its role in the biological process of aging is being recognized (Braidy et al., 2011; Gomes et al., 2013; Lin et al., 2000; Massudi et al., 2012; Scheibye-Knudsen et al., 2014; Zhu et al., 2015). It has been shown that NAD levels decline during chronological aging, and that this decline is both a consequence of the aging process and also a contributor to the development of age-related cellular dysfunction (Braidy et al., 2011; Gomes et al., 2013; Massudi et al., 2012; Scheibye-Knudsen et al., 2014; Verdin, 2015; Zhu et al., 2015). It is possible that a vicious cycle exists in which molecular mechanisms involved in the aging process, such as oxidative stress, DNA damage, senescence, and inflammation, lead to tissue NAD decline which subsequently exacerbates the processes that caused its decline in the first place (Figure 1). To potentially intervene in this vicious cycle it is crucial that we understand the mechanisms that lead to cellular NAD decrease during aging and, in particular, whether the decrease is mediated primarily by changes in its degradation, synthesis, or both. Furthermore, it is critical to understand how oxidative stress, DNA damage, inflammation, and senescence impact cellular NAD metabolism during the aging process. In the current review we will present a critical analysis of this subject, and will provide new mechanistic hypotheses to explain the age-related NAD decline.”