College of Medicine
Department of Neuroscience
Faculty, Chronic Brain Injury
257 Institute for Behavioral Medicine Research
460 Medical Center Drive
Columbus, OH 43210
Dr. Kokiko-Cochran is partially funded by the Chronic Brain Injury program, a part of Ohio State’s Discovery Themes Initiative.
Research Interests: Traumatic brain injury (TBI), Neuroinflammation, Alzheimer’s disease (AD)
Current Research: TBI is a serious concern in civilian and military populations. The frequency of brain injury in professional sports as well as the occurrence of neurodegenerative diseases such as AD, Chronic Traumatic Encephalopathy, and Frontotemporal Dementia indicates that there are serious long-term consequences to even mild and/or repetitive brain injuries. Furthermore, modern military conflicts put soldiers at risk for penetrating and blast-related brain injuries that often correlate with mental health decline, depression, and increased risk for neurodegenerative disease. Although a TBI occurs in a matter of milliseconds, the biological consequences of a brain injury last a lifetime.
Inflammation following TBI is a complex and dynamic response of both the central and peripheral nervous systems, which is influenced by age, sex, injury location and severity, secondary injury cascades, and genetics. Because inflammation occurs after all brain injuries, I consider it an integral component of recovery. However, post-injury inflammation poses both beneficial and detrimental consequences that need to be balanced. Moreover, TBI is not an isolated event within the inflammatory milieu. Accumulating data indicate that pre- and post-injury immune challenges influence the response to brain injury ultimately affecting post-injury pathology and behavioral recovery.
My lab hypothesizes that the brain’s stress response to an immune challenge is compromised following a single TBI. As a result, subsequent life stressors that further challenge the immune system worsen long-tern recovery from TBI. Mounting evidence shows that chronic sleep/wake disruption is a significant stressor that promotes inflammation resulting in brain dysfunction and behavioral impairment. Thus, we predict that post-injury sleep disruption is a significant and understudied stressor that largely influences outcome through inflammatory pathways.
Research Techniques: experimental TBI, behavioral testing, immunohistochemistry, western blot, ELISA, qPCR, flow cytometry
- Tapp, Z.M., Godbout, J.P., and Kokiko-Cochran, O.N. (2019). A Tilted Axis: Maladaptive Inflammation and HPA Axis Dysfunction Contribute to Consequences of TBI. Front. Neurol. 10, 345.
- Kokiko-Cochran, O.N., and Godbout, J. (2018). The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease. Front. Immunol. 9, 672.
- Whiting, M.D., and Kokiko-Cochran, O.N. (2016). Assessment of Cognitive Function in the Water Maze Task: Maximizing Data Collection and Analysis in Animal Models of Brain Injury. Methods Mol. Biol. 1462, 553–71.
- Puntambekar, S.S., Saber, M., Lamb, B.T., and Kokiko-Cochran, O.N. (2018). Cellular players that shape evolving pathology and neurodegeneration following traumatic brain injury. Brain. Behav. Immun. .
- Kokiko-Cochran, O.N., Saber, M., Puntambekar, S., Bemiller, S.M., Katsumoto, A., Lee, Y.-S., Bhaskar, K., Ransohoff, R.M., and Lamb, B.T. (2017). Traumatic brain injury in hTau model mice: Enhanced acute macrophage response and altered long-term recovery. doi.org .
- Kokiko-Cochran, O., Ransohoff, L., Veenstra, M., Lee, S., Saber, M., Sikora, M., Teknipp, R., Xu, G., Bemiller, S., Wilson, G., Crish, S., Bhaskar, K., Lee, Y.-S., Ransohoff, R.M., and Lamb, B.T. (2016). Altered Neuroinflammation and Behavior after Traumatic Brain Injury in a Mouse Model of Alzheimer’s Disease. J. Neurotrauma 33, 625–40.
R01NS109585 Kokiko-Cochran, O.N. (PI)
Agency: National Institutes of Health (NIH), National Institutes of Neurological Disorders and Stroke (NINDS)
Title: Characterizing Sleep Disruption as a Post-Injury Stressor