- PhD, Ohio State University
- MA, University of Richmond
Weil ZM, Karelina K & Corrigan JD, 2019. Does childhood injury cause alcohol misuse: combining preclinical and epidemiological research? Experimental Neurology, 317: 284-290.
Weil ZM, Corrigan JD & Karelina K, 2019.Alcohol use disorders and traumatic brain injury.Alcohol Research: Current Reviews, in press.
Borniger JC, Ungerleider K, Zhang N, Karelina K, Magalang UJ & Weil ZM, 2018.Repetitive brain injury of juvenile mice impairs environmental enrichment-induced modulation of REM sleep in adulthood.Neuroscience, 375: 74-83.
Karelina K, Nicholson S & Weil ZM, 2018.Minocycline blocks traumatic brain injury induced alcohol consumption and nucleus accumbens inflammation in adolescent male mice. Brain Behavior and Immunity, 69: 532-539.
Karelina K, Gaier KR, Weil ZM, 2017.Traumatic brain injuries during development disrupt dopaminergic signaling. Experimental Neurology, 297: 110-117.
Weil ZM & Karelina K, 2017.Traumatic brain injuries during development: implications for alcohol abuse. Frontiers in Behavioral Neuroscience, 11:135.
Karelina K, Gaier KR, Prabhu M, Wenger V, Corrigan TED & Weil ZM, 2017.Binge ethanol in adulthood exacerbates negative outcomes following juvenile traumatic brain injury. Brain, Behavior and Immunity, 60: 304-311.
Weil ZM, Corrigan JD & Karelina K, 2016.Alcohol abuse after traumatic brain injury: experimental and clinical evidence.Neuroscience and Biobehavioral Reviews, 62: 89-99.
Karelina K, Sarac B, Freeman L, Gaier KR and Weil ZM, 2016.Traumatic brain injury and obesity induce persistent central insulin resistance. European Journal of Neuroscience, 43(8): 1034-1043.
Weil ZM, Karelina K, Gaier KR, Corrigan TED & Corrigan J, 2016.Juvenile traumatic brain injury increases alcohol consumption and reward in female mice. Journal of Neurotrauma, 33(9): 895-903.
Karelina K & Weil ZM, 2015.Neuroenergetics of traumatic brain injury. Concussion, 1(2):CNC9. doi: 10.2217/cnc.15.9.
Weil ZM, Gaier K, Karelina K, 2014.Injury timing alters metabolic, functional and inflammatory outcomes following repeated mild traumatic brain injury. Neurobiology of Disease, 70: 108-116.
My main research focus is on identifying environmental and behavioral variables that contribute to neuroprotection or neurodegeneration following traumatic brain injury (particularly injuries that occur early in development). My work (with Dr. Zachary Weil) has begun to identify mechanisms by which mild early life injuries in mice increase vulnerability to long-term consequences such as altered brain metabolism drug/alcohol abuse later in life, as well as reduced capacity for CNS recovery following additional injuries. As a corollary to this work, we have recently begun work to identify potential neuroprotective measures following early life brain injuries. Standard clinical practice for traumatic brain injury typically involves a period of physical and/or cognitive rest until symptom resolution; however, 1) there is little scientific basis for this approach, indeed recent work has shown that this period of rest does little to promote recovery, and 2) symptom resolution is not a good measure of CNS recovery. In direct contrast to the clinical recommendation, it is well established in both basic and clinical research that exercise is profoundly neuroprotective in brain injury, stroke, cardiac arrest, and other forms of CNS injury. Thus, in order to counter the dogma of post-injury rest, we are working to identify 1) the optimal intensity and timing of exercise that promotes recovery after brain injury and 2) the mechanism by which exercise improves cognitive and functional outcomes in mice with brain injury.