SCoBIRC FACULTY

Jonathan Lifshitz, Ph.D.

Assistant Professor,
Spinal Cord & Brain Injury Research Center and Department of Anatomy & Neurobiology

B.S. in Neuroscience from University of California at Los Angeles (1995)
Ph.D. in Neuroscience from University of Pennsylvania (2002)
Postdoctoral training at University of Pennsylvania - Neurosurgery
Postdoctoral training at Virginia Commonwealth University - Anatomy & Neurobiology

Dr. Lifshitz and his lab.

Research Interests

Morbidity and Rehabilitation after Diffuse Traumatic Brain Injury
Moderate, diffuse traumatic brain injury (i.e. concussion) results in multi-focal metabolic and structural pathology in both man and animal, which can disrupt and impair specific neural circuits. Circuit disruption and reorganization could underlie the various symptoms associated with post-traumatic morbidity, broadly categorized as post-concussion syndrome.

Midline fluid percussion is used to produce a diffuse traumatic brain injury in rodents. Structural and functional disruption are explored in neurons, axons, blood vessels and glia throughout the brain, including the brainstem. Experimental approaches explore specific injury-induced neurological dysfunctions:

1. Sensory sensitivity and rehabilitation

In the rodent, the whiskers serve as the primary sensory organ for foraging and survival. Brain-injured rodents demonstrate a startling behavioral response to whisker stimulation, becoming tense and agitated. Whisker stimulation in uninjured animals results in a calming, lulling, soothing effect. To this end, the somatosensory whisker circuit can be exploited using behavioral, pharmacological and histological approaches to evaluate neural circuit disruption, impaired circuit activation and rehabilitation strategies.

2. Vestibular damage contributing to dizziness, nausea and unsteadiness

The vestibular nuclei in the brainstem are vulnerable to the shearing forces that initiate brain injury. Neuronal, glial and vascular damage may explain the acute and chronic neurological deficits associated with balance.

3. Susceptibility of the substantia nigra to diffuse injury forces

Repetitive head injury, typically associated with boxing, results in dementia pugilistica, a neurological condition similar to Parkinson’s Disease. Evidence suggests that the substantia nigra may be particularly vulnerable to neuronal loss and glial activation after diffuse brain injury. Basal ganglia circuit disruption may explain the motor and coordination issues in the chronic brain-injured patient.

The same cellular mechanisms responsible for the injury-induced behavior in rodents could translate to relevant circuits in the human brain, providing treatment or rehabilitation strategies to alleviate morbidity after injury. Therapeutic interventions focus on over-the-counter strategies that would be available to those not necessarily seeking medical care after a head injury.

External Links

University of Kentucky News: YouTube 'Knockout' Videos Yield Clues to Brain Injury
http://uknow.uky.edu/content/youtube-knockout-videos-yield-clues-brain-injury

Jockey Guild Newsletter: Neurological Dysfunction After Brain Injury Arises From New Circuits Formed During Repair
http://www.jockeysguild.com/images/files/newsletters/Newsletter-Vol-2-Iss-4.pdf

YouTube: Fencing Response Found in Sports Injuries
http://www.youtube.com/watch?v=kYkEyvizaIw

Select Publications

McNamara, KCS, A Lisembee, J Lifshitz. (in press) The Whisker Nuisance Task Identifies a Late Onset, Persistent Sensory Sensitivity in Diffuse Brain-Injured Rats. J. Neurotrauma

Hosseini, AH, J Lifshitz. (2009) Brain Injury Forces of Moderate Magnitude Elicit the Fencing Response. Medicine & Science in Sports & Exercise. 41: 1687-97.

Lifshitz, J, BJ Kelley, JT Povlishock. (2007) Perisomatic Thalamic Axotomy After Diffuse Traumatic Brain Injury is Associated with Atrophy Rather Than Cell Death. J. Neuropath and Exp. Neurol.

Lifshitz, J, BM Witgen, MS Grady. (2007) Acute Cognitive Impairment After Lateral Fluid Percussion Brain Injury Recovers by One Month: Evaluation by Conditioned Fear. Behav. Brain Res..

Tran, LD, J Lifshitz, BM Witgen, E Schwarzbach, AS Cohen, MS Grady. (2006) Response of the Contralateral Hippocampus to Lateral Fluid Percussion Brain Injury. J. Neurotrauma 23: 1330-1342.

Witgen, BM, J Lifshitz, MS Grady. (2006) Inbred Mouse Strains as a Tool to Analyze Hippocampal Neuronal Loss after Brain Injury: A Stereological Study. J. Neurotrauma 23: 1320-1329.

Kelley, BJ, O Farkas, J Lifshitz, JT Povlishock. (2006) Traumatic Axonal Injury in the Perisomatic Domain Triggers Ultra-Rapid Secondary Axotomy and Wallerian Degeneration. Exp. Neurol. 198: 350-60.

Farkas, O, J Lifshitz, JT Povlishock. (2006) Mechanoporation Induced by Diffuse Traumatic Brain Injury (DTBI): An Irreversible or Reversible Response to Injury? J. Neurosci. 26: 3130-40.

Lifshitz, J, BM Witgen, ML Smith, E Schwarzbach, MS Grady, AS Cohen. (2005) Regional Hippocampal Alteration Associated with Cognitive Deficit Following Experimental Brain Injury: a systems, network and cellular evaluation. Neurosci. 133: 1-15.

Lifshitz, J, HJ Thompson, N Marklund, MS Grady, DI Graham, DA Hovda, TK McIntosh. (2005) Lateral Fluid Percussion Brain Injury: A 15-year Review and Evaluation [Invited Review]. J. Neurotrauma 22: 42-75.

Grady, MS, JS Charleston, D Maris, BM Witgen, J Lifshitz. (2003) Neuronal and Glial Cell Number in the Hippocampus After Experimental Traumatic Brain Injury: Analysis by Unbiased Stereological Estimation. J. Neurotrauma 20: 929-941.

Wagner, O, J Lifshitz, PA Janmey, M Linden, TK McIntosh, JF Leterrier. (2003) Mechanisms of Mitochondria-Neurofilament Interactions. J. Neurosci. 23: 9046-9058.

Lifshitz, J, TK McIntosh. (2003) Age-Associated Mitochondrial DNA Deletions Are Not Evident Chronically after Experimental Brain Injury in the Rat. J. Neurotrauma. 20: 139-150.

Lifshitz, J, H Friberg, RW Neumar, R Raghupathi, FA Welsh, P Janmey, KE Saatman, T Wieloch, MS Grady, TK McIntosh. (2003) Structural and Functional Damage Sustained by Mitochondria Following Traumatic Brain Injury in the Rat: Evidence for Differentially Sensitive Populations in the Cortex and Hippocampus. J. Cereb. Blood Flow & Metab. 23: 219-31.