The enzyme CD38 drives low NAD+ levels, correlating with a shortened reproductive lifespan and fertility issues in female mice. As female mice age, their CD38 levels increase, and their nicotinamide adenine dinucleotide levels decrease in the ovaries. Genetically modified mice with CD38 deficiency maintain higher NAD+ levels and have more primordial follicles, indicating a potential for a longer reproductive lifespan. CD38-deficient mice have larger litters, which connects increased follicle reserves to enhanced fertility. Supplementation with NAD+ precursors or inhibition of CD38 can elevate ovarian NAD+ levels, possibly slowing ovarian ageing and boosting fertility. The Buck Institute conducted a study on female mice to explore the properties of nicotinamide adenine dinucleotide. The study revealed that the ovaries of normal female mice showed a 2-fold increase in CD38 and a decrease in NAD+ with age. As mice age, a surge in CD38 within the ovaries directly corresponds to a drop in NAD+, signalling a critical factor in the reproductive ageing process. This connection opens new avenues for fertility treatments, highlighting CD38 as a potential target for extending the reproductive lifespan in females. How NAD+ Affects Ovarian Lifespan in Mice The Buck Institute study explains that in young mice lacking CD38, NAD+ levels in ovarian tissues remained high. This finding is pivotal, suggesting a direct link between CD38 activity and NAD+ availability. These mice also preserved a higher count of primordial follicles. Primordial follicles are ovarian reserves that store oocytes. Their abundance is a sign of extended fertility potential. The findings imply that maintaining NAD cell levels could stave off the natural decline in fertility. Higher NAD+ appears to protect the ovarian reserve, extending its lifespan and delaying the reproductive ageing process in mice. These insights are crucial for developing interventions to enhance fertility and slow ovarian ageing. Further research could show whether these findings apply to humans and if there are any NAD supplement side effects. If these results apply to humans, boosting NAD+ could become a strategy to extend women’s reproductive years. Genetic Modification to Prolong Reproductive Health The Buck Institute’s study showed that young, CD38-deficient mice had a more substantial ovarian reserve. They retained more primordial follicles, which are critical to fertility. With more oocytes available, these mice demonstrated an enhanced ability to reproduce over time. This suggests that the presence of CD38 plays a role in the natural decline of fertility. Further, the study linked the number of primordial follicles directly to the mice’s fertility outcomes. The CD38-deficient mice not only had more oocytes but also yielded more offspring. This direct association between genetic modification and increased fertility underscores the potential for reproductive longevity. Moreover, the study hints at the possibility of extending the reproductive period. This could have profound implications for women facing age-related fertility decline. The genetically modified mice provide a model for understanding how changes at the molecular level can influence reproductive health in humans. NAD+ Supplementation as a Fertility Aid NAD+ is a coenzyme found in all living cells and is essential for energy production and cell function. As explained, with age, NAD+ levels drop, and this decline is now linked to reduced fertility. The study found that by boosting NAD cells through supplementation, the ovarian reserve in mice could be protected, potentially extending their reproductive lifespan. The supplementation with NAD+ precursors, such as nicotinamide riboside (NR) or nicotinamide mononucleotide (NMN), showed similar effects to inhibiting CD38. In mice, these supplements led to increased levels of NAD+ in the ovaries, which correlated with a slower rate of ovarian ageing and better fertility outcomes. These findings point towards a non-invasive method to support fertility. Women could use NAD+ supplements to improve their ovarian function and delay the onset of reproductive ageing. These NAD+ supplement benefits would be a significant advancement, given the limited options currently available for managing fertility related to ageing. Implications of Nicotinamide Adenine Dinucleotide for Human Reproductive Lifespan Extension The Buck Institute’s study offers a notable advancement in understanding reproductive ageing. It pinpoints that the enzyme CD38 is a pivotal factor in fertility decline. The study also notes that suppressing CD38 or boosting nicotinamide adenine dinucleotide within ovarian tissues postpones reproductive senescence in mice. As a result, NAD+ supplementation emerges as a promising intervention in boosting ovarian NAD+ and enhancing fertility outcomes in preclinical studies. With this insight, NAD+ supplements stand at the forefront as a non-invasive option that could revolutionise fertility management, especially for women nearing the end of their natural reproductive period. The implications of this research extend beyond fertility alone, hinting at broader applications in women’s health where the best NAD supplement could hinder age-associated decline. If these findings translate effectively from mice to humans, they could significantly impact the future of reproductive medicine.