AOA Honor Medical Society (2020)
PEO Scholar Award (2019)
University of Kentucky Graduate Student Incentive Program Award (2018)
Society for Neuroscience Professional Development Travel Award (2018)
University of Kentucky Graduate School Travel Award (2018)
2nd Annual University of Michigan Massey TBI Summit Invited Mentee
EMBO-FEBS Lecture Course “Mitochondria in Life, Death, and Disease” selected attendee
National Neurotrauma Symposium Sensor Travel Grant Award (2017)
University of Kentucky Graduate School Travel Award (2017)
University of Kentucky Graduate Student Incentive Program Award (2016)
AUPN/NINDS Combining Clinical and Research Careers in Neuroscience Symposium Travel Award (2016)
KSHIRT National Neurotrauma Symposium Registration Award (2016)
NIMH MD/PhD Student Conference/3rd Annual Molecular Psychiatry Meeting Travel Award (2015)
Promoted with High Distinction (M1, M2, M3)
Highest Academic Achievement: Behavioral Basis of Medicine (2013)
Distinguished Portfolio Award: Introduction to Clinical Medicine I (2013)
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BS, Biology, University of Denver, 2004
PhD, Neuroscience, University of Kentucky 2019
I am interested in using pharmacological agents to prevent neurodegeneration and neurologic impairment following experimental TBI, with a specific emphasis on protecting mitochondria and scavenging neurotoxic aldehydes. As my model, I use a severe controlled cortical impact injury. I have evaluated the effects of cyclosporine A (CsA), an immunosuppressant capable of inhibiting mitochondrial permeability transition, on synaptic and non-synaptic mitochondrial bioenergetics following injury. Additionally, I have investigated the effects of a subcutaneous continuous infusion of phenelzine (PZ), an aldehyde scavenger, CsA, and the combination, on mitochondrial bioenergetics, formation of protein-aldehyde conjugates, and spectrin degradation following injury. Currently, I am comparing the effects of PZ, which in addition to being an aldehyde scavenger is also a monoamine oxidase inhibitor (MAOI), to hydralazine (HZ), another aldehyde scavenger, and pargyline (PG), another MAOI, on cortical neurotransmitter and metabolite concentrations, cognitive function, and cortical tissue sparing.
07/2016 – 05/2020
NIH F30 (NINDS) NRSA Predoctoral Fellowship (1F30NS096876-01A1)
Multi-mechanistic protection of mitochondria following traumatic brain injury
Hill RL, Singh IN, Wang JA, KULBE JR, Hall ED. Protective effects of phenelzine
administration on synaptic and non-synaptic cortical mitochondrial function and lipid peroxidation-mediated oxidative damage following TBI in young adult male rats. Exp Neurol 330:113322 (2020)
Hill RL, KULBE JR, Singh IN, Wang JA, Hall ED. Synaptic mitochondria are more susceptible to traumatic brain injury-induced oxidative damage and respiratory dysfunction than non-synaptic mitochondria. Neuroscience 386:265-283 (2018)
KULBE JR, Singh IN, Wang JA, Cebak, JE, Hall ED. Continuous infusion of phenelzine, cyclosporine A, and the combination: evaluation of mitochondrial respiration, oxidative damage, and spectrin degradation following severe controlled cortical impact injury. J Neurotrauma 34(7): 1291-1301 (2018)
KULBE JR and Hall ED. Chronic traumatic encephalopathy-integration of canonical traumatic brain injury secondary injury mechanisms with tau pathology. Prog Neurobiol 158: 15-44 (2017)
KULBE JR, Hill RL, Singh IN, Wang JA, Hall ED. Synaptic mitochondria sustain more damage than non-synaptic mitochondria following traumatic brain injury and are protected by cyclosporine A. J Neurotrauma 34(7): 1291-1301 (2017)
Cebak JE, Singh IN, Wang JA, Hill RL, KULBE JR, Hall ED. Carbonyl Scavenging as an antioxidant neuroprotective strategy for acute traumatic brain injury, in New Therapeutics for Traumatic Brain Injury: Prevention of Secondary Brain Damage and Enhancement of Repair and Regeneration, Heidenreich KA (ed.), Academic Press (2016)
KULBE JR and Geddes JW. Current status of fluid biomarkers in mild traumatic brain injury. Exper Neurol 375: 334-352 (2016)
Barcomb K, Buard I, Coultrap SJ, KULBE JR, O'Leary H, Benke TA, and Bayer KU. Autonomous CaMKII requires further stimulation by Ca2+/calmodulin for enhancing synaptic strength. FASEB J 28(8): 3810-9 (2014)
KULBE JR, Mulcahy Levy JM, Coultrap SJ, Thorburn A, and Bayer KU. Excitotoxic glutamate insults block autophagic flux in hippocampal neurons. Brain research 1542: 12-19 (2014)
Coultrap SJ, Buard I, KULBE JR, Dell'Acqua ML, and Bayer KU. CaMKII autonomy is substrate-dependent and further stimulated by Ca2+/calmodulin. JBC 285: 7930-17937 (2010)