Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterised by reproductive hormone dysregulation involving luteinising hormone (LH) hypersecretion and hyperandrogenism, as well as reduced fertility, due to ovulatory disturbance. In addition, women with PCOS are also predisposed to metabolic disturbances such as obesity, insulin resistance, and dyslipidemia, with an increased risk of cardiovascular disease and type 2 diabetes. Currently, as the origins of PCOS remain unknown, mechanism-based treatments are not feasible and management relies on the treatment of symptoms only. However, if the underlying mechanisms involved in the development of PCOS were uncovered then this would pave the way for the development of new interventions for PCOS. Hyperandrogenism is the most consistent PCOS characteristic, and as androgens mediate their actions via the androgen receptor, we have combined a hyperandrogenised PCOS mouse model with transgenic androgen receptor knockout mouse models to unravel the role of androgens in PCOS. These studies have revealed that androgen actions play an important role in mediating the development of PCOS, and have highlighted the importance of non-ovarian (neuroendocrine and adipose) androgen receptor-mediated androgen actions in the origins of PCOS. In particular, we identified that a specific loss of androgen receptor signalling in the brain protects hyperandrogenised PCOS mice against the development of key reproductive and metabolic PCOS characteristics. These findings support excess androgen receptor-mediated actions in the brain as a key mechanism underpinning the development of PCOS. Hence, our data strongly supports targeting androgen actions in the brain in the development of targeted pharmacological approaches. Collectively these findings provide new insights into how evidence-based interventions may be developed in the future to treat PCOS.