Autism Spectrum Disorders (ASD) is a neurodevelopmental condition, in which individuals exhibit social communicative deficits, repetitive behaviors and restricted interests. Recent estimates approximate 1 in 64 births- the majority being male- with 3 in every 4 confirmed ASD cases. Heightened public awareness, access to quality assessment tools and advancement in scientific research has contributed to increased and accurate diagnoses. Initially thought to have genetic causes, emerging evidence implicates the contribution of environmental factors, thus increasing complexity of elucidating ASD etiology and its underlying mechanisms.
microRNAs (miR) are 15-25 nucleotide long RNA molecules that negatively regulate gene expression in eukaryotic cells. Studies have demonstrated miRs playing essential roles in the onset of both physiological and pathological biological contexts including neurodevelopment, cell differentiation, synaptic plasticity, and behavior. Additionally, emerging evidence of miRs in ASD pathogenesis implicates their involvement in mechanisms essential to brain development and cognition, and behavior.
While research has focused on the independent effects of genes and the environment on ASD development, few studies have investigated their combined effects. My project investigated the effects of a gene-environment interaction model on ASD development and to elucidate the role of microRNA therein. My findings reveal the interaction of these factors gives rise to a unique microRNA signature which coincides with offspring exhibiting behaviors associated with individuals diagnosed with autism spectrum disorders. Taken together, this demonstrates evidence of an interaction paradigm driving dysregulation of mechanisms and behavioral characteristics associated with the ASD phenotype.
Publications
Taeseon Woo, Candice King, Nick I. Ahmed, Madison Cortes, Saatvika Nistala, Matthew J. Will, Clark Bloomer, Nataliya Kibiryeva, Rocio M. Rivera, Zohreh Talebizadeh and David Q. Beversdorf. microRNA as a maternal marker for prenatal stress-associated ASD: evidence from a murine model. Journal of Personalized Medicine, 2023, 13 (9).
Committee Members
Dr. David Schulz
Dr. David Beversdorf
Dr. Elizabeth Bryda
Dr. Anand Chandrasekhar
Candice is currently pursuing opportunities to continue her research in both academia or the private sector.
Speaker Information
Candice King Doctoral Candidate Division of Biological Sciences