Rachel Spooner, PhD
Director, Translational Motor Imaging, Boys Town National Research Hospital
Assistant Clinical Professor, Creighton UniversityPostdoctoral Fellow – Heinrich Heine University Düsseldorf
PhD – Neuroscience, University of Nebraska Medical Center
BA – Biology, Central College
Rachel K. Spooner, PhD, is the Director of the Translational Motor Imaging Laboratory at the Institute for Human Neuroscience. Dr. Spooner is a clinical translational neuroscientist who specializes in using a multidisciplinary fusion of systems biology and neuroscience techniques to comprehensively characterize the neurobiological underpinnings of cognitive-motor dysfunction in healthy and pathological aging cohorts (e.g., Parkinson’s disease: PD, HIV). During her PhD at UNMC, her work was among the first to demonstrate how systemic levels of mitochondrial redox environments and inflammation are related to the neural oscillatory dynamics serving sensorimotor control and cognitive ability in humans. To date, Dr. Spooner has authored more than 40 peer-reviewed publications in premier field-specific and broad audience outlets including PNAS, Brain Behavior and Immunity, Brain Stimulation, NPJ Parkinson’s Disease and Cerebral Cortex.
Dr. Spooner also has an extensive collaborative history providing methodological expertise to laboratories interested in combining invasive and non-invasive brain stimulation such as deep brain stimulation (DBS) and transcranial electrical stimulation (tES) with neurophysiological recordings (e.g., MEG, EEG, LFP). Recently, she utilized combined MEG-DBS recordings in individuals with PD and dystonia to identify neural indices of clinically-effective DBS parameter settings (e.g., orientation, frequency or magnitude of stimulation) to optimally alleviate motor symptoms in clinical populations. The ultimate goal of this research line is to employ personalized dosing of neuromodulation (based on quantifiable changes in brain-behavior dynamics) in order to optimize therapeutic outcomes for age- and disease-related functional decline.
