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Prenatal exposure to common environmental factors affects brain lipids and increases risk of developing Autism Spectrum Disorders

by Christine T Wong, Joshua Wais, Dorota A Crawford


The prevalence of Autism Spectrum Disorders (ASDs) has been on the rise over recent years. The presence of diverse subsets of candidate genes in each individual with an ASD and the vast variability of phenotypical differences suggest that the interference of an exogenous environmental component may greatly contribute to the development of ASDs. The lipid mediator prostaglandin E2 (PGE2) is released from phospholipids of cell membranes and is important in brain development and function; PGE2 is involved in differentiation, synaptic plasticity, and calcium regulation. Our previous review already described extrinsic factors including deficient dietary supplementation and exposure to oxidative stress, infections, and inflammation that can disrupt signalling of the PGE2 pathway and contribute to ASDs. In this review, we describe the structure and establishment of two key protective barriers for the brain during early development: the blood brain barrier and the placental barrier. We then provide the first comprehensive summary of other environmental factors—such as exposure to chemicals in air pollution, pesticides, and consumer products—that can also disturb PGE2 signalling and increase the risk for developing ASDs. We also describe how these exogenous agents are capable of crossing the protective barriers of the brain during critical developmental periods when barrier components are still being formed. This review underlines the importance of avoiding or limiting exposure to these factors during vulnerable periods in development.

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