Shannon Rose, Ph.D.

Research Overview

Dr. Rose’s is actively engaged in hypothesis testing basic and translational pediatric research. Her research program utilizes novel cell biology techniques and metabolomics to study mitochondrial and redox biology in health and pediatric metabolic disorders including autism, obesity, and diabetes.

Dr. Rose’s research builds upon her predoctoral studies with Dr. S. Jill James which focused on systemic glutathione redox imbalance in autism spectrum disorder (ASD) and its association with oxidative stress and mitochondrial dysfunction. Her postdoctoral work with Dr. Richard E. Frye applied the state-of-the-art Seahorse extracellular flux technology to autism to understand the relationship between oxidative stress, environmental exposures, and mitochondrial dysfunction using immune cells from children with ASD and unaffected control children. Her studies distinguished subgroups of children with autism with atypical mitochondrial function and increased susceptibility to oxidant-induced dysfunction. In 2020, Dr. Rose was awarded a multi-principal investigator grant from the United States-Israel Binational Science Foundation. In this study, “Transcriptomic blood biomarkers for ASD diagnostics and precision medicine prognostics,” Dr. Rose and her fellow principal investigators will use a genome-wide RNA sequencing approach to identify transcriptomic biomarkers of ASD and test transcriptomic effects of several candidate therapeutics using a lymphoblastoid cell model of ASD.

Since 2019, Dr. Rose has been funded by the Center for Childhood Obesity Prevention (CCOP), (P20GM109096; PI: Weber), an NIH-funded Center of Biomedical Research Excellence (COBRE) at ACRI, to assess the association between inflammation and metabolic pathways used by immune cells to make ATP in children spanning a wide range of body mass index and metabolic health. In her current CCOP study, Dr. Rose is testing the hypothesis that compared to healthy weight children, obese children with elevated biomarkers of inflammation will have fewer regulatory T cells, and their helper T cells will be skewed towards an activated immune and metabolic phenotype. To test this hypothesis, Dr. Rose is conducting immune and metabolic profiling of blood samples from human subjects as well as utilizing a mouse model of diet-induced obesity.