The molecular biology of ageing has captured the public imagination, with the idea that within our lifetimes, new drugs could improve late-life health and even extend human lifespan. In reality, the clinical translation of basic discoveries in this field are hampered by the practical realities of clinical trial design, leading to trials for new geroprotective drug interventions in age-related indications such as cardiovascular disease, dementia and other common conditions of ageing. These ignore a much earlier event in the life history of mammals: female infertility, with declining oocyte quality occurring far earlier than declines in any other tissue due to the non-renewable nature of the ovarian reserve. Here, I will cover my lab’s key findings in the biology of reproductive ageing, including our discovery of declining levels of the redox cofactor NAD+ in age-related female infertility, and its subsequent clinical translation, and applications in other aspects of reproductive health, including chemotherapy induced ovarian toxicity. I will also describe new mechanistic insights in NAD+ metabolism from stable isotope tracing, and its applications in clinical translation. Finally, I will present the age-mismatched re-aggregation of “heterochronic cumulus oocyte complexes” as a new, unbiased approach for discovering factors that could rejuvenate oocyte quality during ageing, and answer fundamental “chicken and egg” questions around the role of somatic versus germ cell ageing in reproductive decline.