Sarah Latchney, assistant professor of biology and neuroscience, has recently been published in Developmental Neurobiology titled, “Persistent organic pollutants at the synapse: Shared phenotypes and converging mechanisms of developmental neurotoxicity.”
In this article, Latchney reviewed the literature that supports a hypothesis that the neuronal synapse – the junction between neurons – is a vulnerable target to a significant source of man-made environmental pollutants known as persistent organic pollutants. These ubiquitous chemicals include polychlorinated biphenyls, polychlorinated dibenzodioxins, and polybrominated diphenyl ethers. The article summarizes published evidence suggesting that there are shared toxicological mechanisms that may underlie structural and functional changes within the synapse and can predispose the developing fetus or child to neurodevelopmental disorders. With more than 80,000 chemicals registered for commercial use with the U.S. Environmental Protection Agency, understanding converging mechanisms of action will aid in defining future research to increase our understanding of how persistent organic pollutants may modify synaptic structure and function and contribute to neurodevelopmental disorders that are characterized by synaptic pathology.