Defective Placentas Could Cause Improper Brain Development, Brain Injury, Increased Inflammatory Response Due to a Dysregulated Immune System, and Oxidative Stress
Defective placentation describes several syndromic manifestations that can adversely affect fetal brain development. These conditions include placental abruption, term preeclampsia with a small-for-gestational-age (SGA) infant, preterm preeclampsia, and spontaneous preterm birth. A recent Swedish study investigated the relationship between defective placentation syndromes and the incidence of autism spectrum disorder (ASD). This population-based cohort study examined 1,645,455 non-malformed singleton infants born in Sweden between 2000 and 2016. The research also included up to 17 years of follow-up information on participants. The study’s design was straightforward. It compared ASD rates for children exposed and unexposed to defective placentation syndromes. Additionally, a sibling-controlled analysis for 1,092,132 full siblings was included in the research. The results showed that ASD rates were increased in children of mothers who experienced placental abruption. Higher ASD rates were also found in children of mothers with preeclampsia, especially in term preeclampsia with SGA and preterm preeclampsia < 34 weeks. Rates of ASD increased with decreased gestational age, showing the highest rates for the very/extremely preterm birth infants. The research team behind the study was puzzled by preeclampsia’s effect on the offspring. They found consistent associations between ASD and late preeclampsia with SGA or preterm preeclampsia. However, a substantial proportion of the link between ASD and preeclampsia was not mediated through preterm birth. This suggests that preeclampsia may have a distinct role in developing autism. The authors believe the association could represent an effect of defective placentation on brain development. They also propose that the link could be due to brain injury from conditions that accompany the pathophysiology of preeclampsia, such as increased inflammatory response through dysregulated immune activation and oxidative stress.
