Abstract
In the United States, 1 in 6 children are diagnosed with a neurodevelopmental disorder (NDD)—a heterogeneous group of disorders resulting from impaired brain development. Evidence indicates that NDDs have both genetic and environmental etiologies. In fact, the gene-environment hypothesis posits that it is the combination of NDD risk genes and environmental factors that often confer the greatest risk of NDDs. Our research aims to examine how one prevalent environmental factor—bisphenol A (BPA)—affects neurodevelopment in the Fragile X Syndrome Model of Drosophila. Fragile X mental retardation 1 (FMR1) is an NDD associated genetic factor that causes Fragile X syndrome and is the most common single-gene cause of autism spectrum disorder (ASD). Bisphenol-A (BPA) is a high-volume chemical that is produced worldwide and used in the synthesis of polycarbonate plastics and epoxy resins. BPA has well established roles as an endocrine disrupting chemical (EDC) and emerging studies indicate that BPA may also impact neurodevelopment. Our study will determine how developmental exposure to BPA impacts synapse formation—a critical developmental process—on its own, or in combination with the Drosophila ortholog of FMR1 (dfmr1).