Nicotinamide adenine dinucleotide (NAD+) is an essential metabolic co-factor regulating energy synthesis and developmental processes in oocytes and early embryos. Oocyte NAD+ levels decline during reproductive ageing, which is linked to suboptimal embryo development. We showed previously that oral supplementation with the NAD+ precursor, nicotinamide mononucleotide (NMN) in aged mice restores reproductive function. Here, we hypothesized that NAD+ synthesis and accumulation in oocytes is important for embryo development. Firstly, we inhibited NAD+ synthesis with 30 µM FK866 in mouse GV oocytes either during in-vitro maturation (IVM) and/or in mature oocytes during IVF. Depletion of NAD+ in oocytes during IVM significantly reduced day 5 blastocyst rates by 30%, whereas depletion during IVF had no effect. This suggests sufficient oocyte NAD+ reserves are required for healthy embryo development. We investigated this further by supplementing oocytes from aged mice with NMN during IVM, which improved blastocyst development by 10% compared to untreated aged oocytes. To explore the underlying mechanisms, we investigated NAD+ turnover in oocytes and embryos by conducting a pulse-chase experiment using liquid chromatography-mass spectrometry (LC-MS). Deuterium-4 labelled nicotinamide was supplemented to either GV oocytes, 2-cell embryos or compacted embryos for 16 hours. Our data revealed that oocytes accumulate excess NAD+ and its precursors during meiotic maturation, with ~30% of total NAD+ in blastocysts derived from maternal stores. Previous studies have shown that NAD+ is rapidly consumed in the first 24 hours of embryo development. Our LC-MS data show that embryos can replenish NAD+ levels but only after reaching the two-cell stage. Together, our findings demonstrate that maternally stored NAD+ and its precursors are critical for supporting embryo development. This work also further highlights the potential NAD+ supplementation strategies for women of advanced maternal age undergoing IVF.