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

Research Interests

Somatosensory system disruption and rehabilitation after brain injury
Moderate, diffuse traumatic brain injury (i.e. concussion) results in multi-focal histological pathology in both man and animal, which can disrupt specific neural circuits. Circuit disruption gives rise to the array of symptoms associated with post-traumatic morbidity and broadly categorized as post-concussion syndrome. In the rodent, the whiskers serve as the primary sensory organ for foraging and survival. The diffuse axonal, vascular, membrane and neuronal perturbations that occur in response to experimental traumatic brain injury (fluid percussion injury) result in a startling behavioral response to whisker stimulation. Whereas whisker stimulation in an uninjured animal results in a calming and lulling effect, brain-injured animals become tense and agitated to identical stimulation. 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 possible rehabilitation strategies. 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.

Select Publications

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.