One in ten women of reproductive age is likely to have polycystic ovary syndrome (PCOS), a complex endocrine disorder that affects reproductive, metabolic, cardiovascular and psychological health. PCOS is defined by ovarian dysfunction, including the diagnostic features of androgen excess, reduced or absent ovulation, and polycystic ovarian morphology. However, two seminal studies in the late 1990s challenged the primary role of the ovary in PCOS, and instead implicated intrinsic features in the brain, specifically the gonadotropin-releasing hormone (GnRH) neuronal network, as central to PCOS pathology.

Usually, the reproductive axis features reciprocal communication between a network of neurons in the brain (the GnRH neuronal network) and the gonads. Hormones released from the hypothalamus, pituitary and gonads (HPG) are key parts of this communication. Patterned, pulsatile release of GnRH from the hypothalamus promotes pituitary release of luteinizing hormone (LH) and follicle-stimulating hormone, which together regulate ovarian function. Gonadal hormones, in turn, provide essential feedback signals to the brain and pituitary to shape GnRH and LH release.