Neuroendocrine Impairments in PCOS: Pathogenesis and Therapeutic Interventions

Abstract

Anovulatory infertility is primarily caused by the endocrine complication known as polycystic ovarian syndrome (PCOS). PCOS, which is characterized by hyperandrogenism, irregular periods, and polycystic ovaries, which is a multifaceted condition that is unlikely to have a single common cause. The brain is becoming a key candidate in both the ontogeny and pathophysiology of PCOS, despite the fact that it is still typically thought of as an ovarian disease. Impaired gonadal steroid hormone negative feedback to the GnRH neuronal network in the brain that controls fertility is a crucial pathogenic characteristic of PCOS. The primary characteristic of PCOS, androgen excess, is linked to this impairment. It is believed that hyperactivity of the neuroendocrine axis regulating fertility is caused by impaired steroid hormone feedback to GnRH neurons, creating a vicious cycle of excess androgen and reproductive failure. Due to the enormous complexity of researching the human brain, decades of clinical research have failed to identify the mechanisms behind this disability. We have only lately started to understand the function of the brain in the onset and evolution of PCOS, thanks to the creation of preclinical models of the condition. The research presented here shows how crucial the brain is to PCOS ontogeny and pathophysiology and emphasizes the need for a deeper comprehension of the underlying mechanisms.