NSGR - Early Rehabilitation Attenuates Late-Onset Symptoms and Restores Circuit Function in a Preclinical Traumatic Brain Injury Model - Theresa Currier Thomas, PhD

At the end of this presentation, participants should be able to:

• Identify key aspects of preclinical models of traumatic brain injury (TBI) that are valuable for studying mechanisms, prevention, and treatment strategies for late-onset symptoms.
• Analyze the contribution of maladaptive circuit reorganization as a pathophysiological process underlying late-onset neurological deficits after concussive brain injury/diffuse axonal injury.
• Evaluate the efficacy of early circuit-directed rehabilitation for driving adaptive neuroplasticity and mitigating late-onset neurological deficits and associated circuit function.

About this presenter:

Theresa Currier Thomas, PhD
Director, Translational Neurotrauma and Neurochemistry Research Lab
Barrow Neurological Institute at Phoenix Children's
Departments of Child Health and Translational Neurosciences

Research Investigator
Phoenix VA Health Care System
Associate Professor, Scientist Track
Barrow Neurological Institute

Associate Professor
Biomedical Sciences Program
Midwestern University – Glendale

Theresa Currier Thomas, PhD in an Associate Professor and Director of the Translational Neurotrauma and Neurochemistry Research Lab in the Department of Child Health at the University of Arizona, College of Medicine–Phoenix. My research focuses on late-onset morbidity following traumatic brain injury (TBI), particularly how diffuse axonal injury (DAI)-induced circuit reorganization impacts long-term recovery. My lab specializes in the midline fluid percussion injury (mFPI) model to investigate mechanisms of chronic neuroplasticity, gliosis, and circuit dysfunction that contribute to persistent behavioral and cognitive deficits.

With over 25 years of experience in preclinical neuroscience research, I have developed expertise in neurotransmission (25y), traumatic brain injury (18y), neuroendocrinology, neuroplasticity, synaptogenesis, gliosis, aging, Parkinson’s disease, aging-with-injury, and sex differences. My work integrates multidisciplinary approaches to elucidate mechanisms of circuit reorganization and identify therapeutic targets to improve long-term recovery.

I have a proven track record in leading, executing, and publishing independent and collaborative research projects. My early investigator award from the Arizona Biomedical Research Centre resulted in 9 publications, establishing the foundation for identifying hypothalamic-pituitary-adrenal (HPA) axis dysregulation in our preclinical model of DAI. My first NIH R01 has generated over 20 publications, demonstrating that late-onset behavioral morbidity correlates with thalamic circuit dysfunction and is responsive to early rehabilitation as a prophylactic intervention. Additional work has uncovered TBI-induced disruption of estrous cycles, neurotransmission deficits, chronic thalamic neurodegeneration, and glial-specific phenotypes, highlighting the thalamus as an epicenter for behavioral morbidity.

In addition to my research, I am committed to mentorship and scientific advancement, having successfully mentored over 50 trainees and authored over 45 peer-reviewed publications and 12 book chapters.