Placental ageing and cell senescence contribute to the pathophysiology of preterm birth, fetal growth restriction and stillbirth. However, the molecular mechanisms underlying placental ageing with respect to poor birth outcomes are poorly understood. Mitochondria contribute to age-related diseases in other tissues through production of reactive oxygen species and mechanisms that induce cellular senescence. The aim of this study was to investigate the expression of markers of mitochondrial dysfunction, cellular senescence and placental ageing in pre-term, term and post-date (overdue) placentae to determine possible associations. Preterm (34-36 weeks' gestation, n=6-7), term (39-40 weeks' gestation, n=6-7) and post-date (41-42 weeks' gestation, n=6-7) human placental samples were taken at delivery in Victoria and Queensland. Following RNA extraction, qRT-PCR was utilised to measure 24 genes to assess the profile of cellular stress and dysfunction associated with gestational ageing. Subsequent protein extraction and western blotting was performed on proteins of interest; TFAM, SIRT1, SIRT3, P53, PARKIN. For both mRNA and protein analyses, pre-term and post-date samples were assessed relative to term controls. Placental ageing genes TERF1 and EP300 were decreased, whilst VWA5A was increased. Genes associated with mitochondrial dysfunction CDKN1C, FOXO1, TOLLIP and SIRT1 were significantly decreased. Western blot found age-related marker p53 was significantly decreased in pre-term placenta, whilst significantly increased in post-date placentae. Mitochondrial dysfunction markers SIRT1 and TFAM were decreased in pre-term placenta, whilst increased in post-date placentae (p<0.05). This study showed that some markers of placental ageing and mitochondrial dysfunction change across pregnancy and may be upregulated in 'older' placentas, which may contribute to senescence. This is important because it is known that stillbirth rates rise substantially at term gestation. Further studies will assess whether pregnancy complications such as preeclampsia and fetal growth restriction may be associated with premature placental ageing and mitochondrial dysfunction and the association with cellular senescence.