Background: Bisphenol A (BPA) is one of the highest volume chemicals produced worldwide. It has
recognized activity as an endocrine disrupting chemical and has suspected roles as a neurological and
reproductive toxicant. It interferes in steroid signaling, induces oxidative stress, and affects gene
expression epigenetically. Gestational, perinatal and neonatal exposures to BPA affect developmental
processes, including brain development and gametogenesis, with consequences on brain functions,
behavior, and fertility.
Methods: This review critically analyzes recent findings on the neuro-toxic and reproductive effects of
BPA (and its analogues), with focus on neuronal differentiation, synaptic plasticity, glia and microglia
activity, cognitive functions, and the central and local control of reproduction.
Results: BPA has potential human health hazard associated with gestational, peri- and neonatal
exposure. Beginning with BPA’s disposition, this review summarizes recent findings on the neurotoxicity
of BPA and its analogues, on neuronal differentiation, synaptic plasticity, neuro-inflammation, neuro-
degeneration, and impairment of cognitive abilities. Furthermore, it reports the recent findings on the
activity of BPA along the HPG axis, effects on the hypothalamic Gonadotropin Releasing Hormone
(GnRH), and the associated effects on reproduction in both sexes and successful pregnancy.
Conclusion: BPA and its analogues impair neuronal activity, HPG axis function, reproduction, and
fertility. Contrasting results have emerged in animal models and human. Thus, further studies are needed to better define their safety levels. This review offers new insights on these issues with the aim
to find the “fil rouge”, if any, that characterize BPA’s mechanism of action with outcomes on neuronal
function and reproduction.