Abstract

Prenatal depression and preeclampsia (PE) are well-known risk factors of maternal and fetal mortality and morbidity. In recent years, there are emerging evidence suggesting that prenatal depression and PE could be environmental risk factors for several neurodevelopment disorders of offspring. Prenatal depression and PE were also found to be risk factors of each other. At present, the mechanism (s) of how prenatal depression and PE affect one another and their roles in the development of maternal and fetal adverse outcomes are uncertain. In this review, we outline the most recent clinical studies on the effects of prenatal depression and PE on the neurodevelopmental outcomes of offspring, as well as the plausible mechanism(s) of how these two maternal conditions affect each other and their roles in the neurodevelopment of offspring, including inflammation, oxidative stress, and maternal immune activation. We postulate that the overproduction of pro-inflammatory cytokines and increased cortisol levels in maternal depression can alter fetal neurodevelopment, and the autonomic nervous system dysfunction caused by maternal depression may accelerate heart rate and elevate blood pressure in mothers. Similarly, in PE, the elevated inflammation and exaggerated oxidative stress in the mothers, placenta, and fetus could negatively affect maternal depression on and impair the neurodevelopment of offspring. Further studies are needed to examine the combined effects of prenatal depression and PE on the health outcomes of mothers and offspring, to explore the mechanism of maternal depression in the development of PE and to investigate their roles in the neurodevelopment of offspring.

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