Prenatal exposure and fetal programming of schizophrenia

Abstract

Schizophrenia (SCZ) is a neurodevelopmental disorder, which results to cognitive dysfunction and memory decline. Maternal undernutrition during fetal development alters epigenomic programming, and this might result to SCZ in offspring later in life because of the disruption of fetal brain development and synaptogenesis. Maternal stress, exposure to teratogens and neurotoxic agent, hypoxia, and viral infection alters fetal neurodevelopmental mechanisms because of an increase in inflammatory proteins. Interleukin 8 and tumor necrosis factor released due to stress and infection increase the risk of offspring developing SCZ later in life. Having infections linked to Toxoplasma gondii, Chlamydia, and some pathogens seropositivity during pregnancy or the period preceding childbirth are high-risk factors for offspring to develop SCZ later in life. This review was conducted by extracting papers using key terms indicating Schizophrenia, fetal programming of neurodevelopmental disorders, maternal undernutrition, maternal immune activation, and genome-wide studies through PubMed, Science Direct, PsychINFO, Medline, Web of Science, and Google Scholar. Maternal Stress was found to induce hypermethylation resulting to poor expression of reelin, which causes a reduction in GABAergic neurons in animal models. In vivo animal experimentation indicated that poor maternal care, unfavorable environmental factors, and conditions produce aberrant deoxyribonucleic acid methylation patterns at various gene loci in the medial prefrontal cortex of the brain, thus altering and modifying the network of genes involved in mental activities. However, the epigenomic mechanisms behind the fetal programming of SCZ have not been fully understood; more facts could be unraveled in the future.