Dr. Ngwenya is an Assistant Professor in the Departments of Neurosurgery and Neurology & Rehabilitation Medicine at University of Cincinnati. She is also the Director of the Neurotrauma Center at the University of Cincinnati Gardner Neuroscience Institute. Dr. Ngwenya earned her joint MD, PhD degree from Boston University School of Medicine. Her graduate thesis defined the generation and maturation process of adult born neurons in the hippocampal dentate gyrus of young and aging rhesus monkeys. She then underwent training in Neurological Surgery at The Ohio State University Wexner Medical Center. Her research efforts during residency demonstrated that the process of new neuron generation is abnormal after a rodent model of traumatic brain injury. After completion of residency, she worked as a Clinical Instructor at the University of California San Francisco, San Francisco General Hospital while obtaining fellowship training in Neurotrauma and Neurocritical Care. Dr. Ngwenya joined University of Cincinnati in 2016 as an academic neurosurgeon who specializes in neurotrauma, and also treats patients with general neurosurgery conditions. She is actively engaged in clinical trials and translational research. Her neurotrauma laboratory focuses on mechanisms underlying poor cognitive recovery, with an emphasis on adult neurogenesis, and an ultimate goal of improving outcomes in patients with traumatic brain injury.
Identifying the genetic risk underlying poor cognitive recovery after traumatic brain injury.
Traumatic brain injury (TBI) affects 2.8 million people in the United States annually,1 many of whom have untreated impaired cognitive recovery. While injury factors are important, pre-injury conditions, specifically psychiatric history, negatively influence outcome.2,3 Yet the genetic risk that pre-injury psychiatric conditions bestow upon outcome after TBI has been largely disregarded in both clinical and laboratory studies. Defining the genetic alterations in psychiatric illness that contribute to poor outcome after TBI will lead to discovery of therapeutic targets for a large population of currently untreated individuals and advance a precision medicine approach to TBI treatment. Patients with major depression have cognitive difficulties and hippocampal pathology.4 The inbred rat strain Wistar Kyoto (WKY) is a well-characterized, commercially available rodent model of depression that shows decreased locomotor activity, increased stress response, and learned helplessness.5,6 In addition to the behavioral phenotype of WKY rats, these rats show a congenital decrease in hippocampal adult neurogenesis, illustrated by defects in the ability to create new neurons in the dentate gyrus (DG).7 Due to the importance of the hippocampus in learning and memory, pre-injury hippocampal dysfunction is a culprit for poor cognitive recovery after TBI. Our long-term goal is to identify the substrates that underlie discordant cognitive recovery after TBI. The hippocampus shows damage after TBI, with decreases in cell number and function. We have shown altered hippocampal neurogenesis following the lateral fluid percussion injury (LFPI) model of TBI, with abnormal increases in neurons and defects in integration of new cells. Thus, converging evidence suggests that post-injury hippocampal dysfunction is also an integral factor in recovery. An individual that is genetically predisposed to hippocampal dysfunction pre- injury due to psychiatric illness may be increasingly susceptible to poor cognitive recovery post- injury. Understanding how genetic risk impacts TBI recovery will lead to identification of novel substrate targets for development of patient-centered therapeutics.