Abstrait

Origin of Mental illness in Fetus

Erin Mazhar

Due to significant clinical and research gaps, the effect of infections and inflammation during pregnancy on the developing fetal brain is still poorly understood. Toxoplasma gondii, rubella virus, Cytomegalovirus (CMV), and herpes simplex virus are the classic infectious TORCH pathogens that are known to be directly teratogenicity. However, new evidence suggests that these infections are just one extreme end of a much wider range of injuries. Prenatal exposure to a variety of viral and bacterial infections, or simply inflammation, may subtly alter fetal brain development, resulting in neuropsychiatric consequences for the child later in life, according to the evidence presented here. Over 30 years ago, a connection was made between influenza infections in pregnant women and an increased risk of schizophrenia in their children. Since then, there is evidence that a variety of infections during pregnancy may also make the child more likely to have autism spectrum disorder and depression. After that, research on animal models showed that both infections during pregnancy and inflammation can damage neurons and neural progenitor cells directly or indirectly by activating microglia and astrocytes, which can cause cytokine production and oxidative stress. Placental serotonin production can also be altered by infectious exposures, which can disrupt neurotransmitter signaling in the developing brain. It is difficult to detect these subtle brain injuries in a clinical setting. Our construct for defining teratogenic infections in pregnancy (such as TORCH) based on congenital anomalies is insufficient to capture the full adverse impact on the child because the neuropsychiatric impact of perinatal infections or inflammation may not be known until decades after birth.