Gamete/Embryo-Fetal Origins of Mental Disorders

Abstract

The mechanisms of normal development of the central nervous system could be modulated by a variety of spatial and temporal factors. Neurodevelopmental disorders may originate during fetal life because the feto-maternal environment is vulnerable to negative intrauterine and extrauterine factors, such as maternal smoking, alcohol, nutrition, endocrine disruptors, exposure to pesticides such as chlorpyrifos, exposure to drugs such as terbutaline, maternal teratogenic alleles, psychosocial stress, and infection during pregnancy, as well as preterm birth. As a consequence, the process of fetal neurodevelopment, which involves cell programs, developmental trajectories, synaptic plasticity, and oligodendrocyte maturation, could be adversely affected [1, 2]. Possible mechanisms include changes in neurodevelopment, changes in the set points of neuroendocrine systems caused disruption to placental function, environmental toxin cross the placental barrier and early programming effects, and, there is evidence that prenatal adversity interacts with intrinsic genetic factors, and, extrinsic, postnatal, environmental factors [3]. Meanwhile there is also accumulating evidence suggesting that epigenetic changes may mediate programming effects at a molecular level during embryonic and fetal development [4]. In this chapter, we will discuss the evidence related to Embryo-fetal origins of mental disorders.