Kate Karelina Weil, PhD

Research Interests

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.

Publications

PubMed

Google Scholar

Relevant Publications:

[2023]

• Weil, Z.M., Ivey, J.T., Karelina, K. 2023. Putting the mind to rest: a historical foundation for rest as a treatment for traumatic brain injury. Journal of Neurotrauma. doi: 10.1089/neu.2022.0363

[2021]

• Weil, Z.M., Karelina, K., Whitehead, B., Velazquez Cruz, R., Oliverio, R., Pinti, M., Nwafor, D.C., Nicholson, S., Fitzgerald, J., Hollander, J., Brown, C.M., Zhang, N., DeVries, A.C. 2021.  Mild traumatic brain injury increases vulnerability to cerebral ischemia in mice.  Experimental Neurology, 342:113765. doi:10.1016/j.expneurol.2021.113765.

• Karelina, K., Schneiderman, K., Shah, S., Fitzgerald, J., Velazquez Cruz, R., Oliverio, R., Whitehead, B., Yang, J., Weil, Z.M. 2021.  Moderate intensity treadmill exercise increases survival of newborn hippocampal neurons and improves neurobehavioral outcomes following traumatic brain injury.  Journal of Neurotrauma, 38(11): 1858-1869. 

[2019]

• Weil, Z.M., Karelina, K. 2019. Lifelong consequences of brain injuries during development: from risk to resilience.  Frontiers in Neuroendocrinology, 55:100793. doi:10.1016/j.yfrne.2019.100793.

[2018]

• Karelina, K., Nicholson, S., Weil, Z.M. 2018.  Minocycline blocks traumatic brain injury induced alcohol consumption and nucleus accumbens inflammation in adolescent male mice.  Brain Behavior and Immunity, 69: 532-539.

[2017]

• Karelina, K., Gaier, K.R., Weil, Z.M. 2017.  Traumatic brain injuries during development disrupt dopaminergic signaling.  Experimental Neurology, 297: 110-117.

[2016]

• Karelina, K., Sarac, B., Freeman, L., Gaier, K.R., Weil, Z.M. 2016.  Traumatic brain injury and obesity induce persistent central insulin resistance.  European Journal of Neuroscience, 43(8): 1034-1043.

• Karelina, K., Weil, Z.M. 2016.  Neuroenergetics of traumatic brain injury.  Concussion, 1(2):CNC9. doi: 10.2217/cnc.15.9.

[2015]

• Karelina, K., Liu, Y., Alzate-Correa, D., Wheaton, K.L., Hoyt, K.R., Arthur, J.S.C., Obrietan, K. 2015.  Mitogen and stress-activated kinases 1/2 regulate ischemia-induced hippocampal progenitor cell proliferation and neurogenesis. Neuroscience, 285: 292-302.

[2014]

• Karelina, K., Alzate-Correa, D., Obrietan, K. 2014.  Ribosomal S6 kinase (RSK) regulates ischemia-induced progenitor cell proliferation in the adult mouse hippocampus.  Experimental Neurology, 253: 72-81. Cover Image.