title: Prenatal exposure to common environmental factors affects brain lipids and increases risk of developing autism spectrum disorders.
abstract: 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. The previous review already described extrinsic factors, including deficient dietary supplementation, and exposure to oxidative stress, infections and inflammation that can disrupt signaling of the PGE2 pathway and contribute to ASDs. In this review, the structure and establishment of two key protective barriers for the brain during early development are described: the blood-brain barrier; and the placental barrier. Then, the first comprehensive summary of other environmental factors, such as exposure to chemicals in air pollution, pesticides and consumer products, which can also disturb PGE2 signaling and increase the risk for developing ASDs is provided. Also, 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 is described. This review underlines the importance of avoiding or limiting exposure to these factors during vulnerable periods in development.
authors.affiliation: School of Kinesiology and Health Science, York University, Toronto, ON, Canada, M3J 1P3.|Neuroscience Graduate Diploma Program, York University, Toronto, ON, Canada, M3J 1P3.
authors.forename: Christine T
authors.initials: CT
authors.lastname: Wong
authors.affiliation: School of Kinesiology and Health Science, York University, Toronto, ON, Canada, M3J 1P3.
authors.forename: Joshua
authors.initials: J
authors.lastname: Wais
authors.affiliation: School of Kinesiology and Health Science, York University, Toronto, ON, Canada, M3J 1P3.|Neuroscience Graduate Diploma Program, York University, Toronto, ON, Canada, M3J 1P3.|Department of Biology, York University, Toronto, ON, Canada, M3J 1P3.
authors.forename: Dorota A
authors.initials: DA
authors.lastname: Crawford
mesh_terms: D000818:Animals; D000067877:Autism Spectrum Disorder / Q000378:metabolism*; D001812:Blood-Brain Barrier / Q000196:embryology / Q000378:metabolism*; D001921:Brain / Q000196:embryology / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism; D002462:Cell Membrane / Q000737:chemistry / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism*; D004781:Environmental Exposure / Q000009:adverse effects*; D005260:Female; D006801:Humans; D010920:Placenta / Q000196:embryology / Q000378:metabolism*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism*; D012307:Risk Factors; D015398:Signal Transduction
chemical_list: D002352:Carrier Proteins; D015232:Dinoprostone
keywords: autism; blood brain barrier; chemicals; lipids; prostaglandin