Could We Hack Women’s Biological Clock? A Mitochondrial Hypothesis

mtDNA is constantly replicating during oocyte maturation, but the number is stable after maturation (metaphase II oocytes). mtDNA level in human oocytes is inversely associated with maternal age and ovarian reserve clinical indicators [5]. Mountains of evidences show that older women’s embryos have higher levels of mtDNA, which is correlated with implantation failure, and there is a threshold level of mtDNA above which implantation never occurred [6]. On the other hand, mtDNA level has found raised in aneuploid embryos compared to euploid embryos, independently of the maternal age [7]. That increased mtDNA has been correlated with elevated metabolism and reduced viability, consistent also with the “quiet embryo” hypothesis. This hypothesis proposes that the viability of early mammalian embryos is associated with a metabolism that is quiet rather than active [7-9]. The process of disjunction requires a significant amount of energy, provided by ATP from the mitochondria, and therefore, mitochondrial dysfunction is associated with oocyte aging and increased incidence of aneuploidy of maternal origin [10,11]. Duran et al. [5] have proposed that mtDNA quantification was more closely associated with Follicle-Stimulating Hormone (FSH) predicted reproductive age than with chronological age.