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Brain Injury & Neuroprotection Research


Acute brain injury caused by stroke, cardiac arrest, transient hypoxia and head trauma affects over 1 million people each year in the US alone. Our mission is to improve the survival and quality of life for brain injury victims. Our approach includes the use of both basic and translational research directed at understanding the molecular mechanisms of neural cell death. We also use tissue and fluid samples obtained from traumatic brain injury patients to validate the mechanisms elucidated from our animal models and to identify accurate biomarkers of acute neurodegeneration.

Focus of study

Relationships between excitotoxicity, cellular calcium overload, metabolic failure, and oxidative stress with emphasis on the role that mitochondrial dysfunction plays in both necrotic and apoptotic cell death.

Research Topics

  • Brain mitochondrial physiology and bioenergetics
  • Oxidative stress
  • Cerebral energy metabolism
  • Necrotic and apoptotic neural cell death
  • Brain inflammation
  • Translational research utilizing animal models of cerebral ischemia, traumatic brain injury, neonatal asphyxia
  • Development of clinically feasible neuroprotective interventions

View our Publications 


  • Small and large animal surgical facilities
  • Fluorescence live cell imaging workstation with environmental control
  • Histology workstation with advanced stereology
  • Anoxia chamber
  • Multi-incubator cell culture system with independent oxygen controls


  • Julie Proctor, MS; Lab Supervisor
  • Chunli Lui, MD, MS: Lab Specialist
  • Parisa Rangghran, MS: Research Assistant
  • Juliana Medina, Research Assistant, Laboratory Animal
  • Ashley Moore, Research Assistant, Laboratory Animal
  • Prathistha Tamrakar, Post-Doctoral Fellow
  • Brian Roelofs, Post-Doctoral Fellow
  • Lindsey Lund, Laboratory Technician
  • Tyler Demarest, PhD (Student)
  • Sausan Jaber, PhD (Student)
  • Evan Bordt, PhD (Student)

Faculty Researchers

Selected Images

Neuron-specific Conditional Expression of a Mitochondrially Targeted Fluorescent Protein In Mice

Mitochondrially-targeted eYFP(green) is shown in CA1 pyramidal cells whose cell bodies were labeled with anti-NeuN antibbodies (red). 

Normoxic Resuscitation After Cardiac Arrest Protects Against Hippocampal Oxidative Stress, Metabolic Dysfunction, and Neuronal Death

Following 10 min of v-fib cardiac arrest, chloralose-anesthetized animals were resuscitated on either 100% O2 (Hyperoxic) or 21% O2 (Normoxic). After 1 hr, ventilatory adjustments maintained normal PaO2 in both groups. After 2 hr, the brains were perfusion-fixed and processed for GFAP (red) and nitrotyrosine (green) immunostaining. The dramatic decrease in nitrotyrosine immunostaining in the hippocampus of the Normoxic compared to the Hyperoxic animal indicates protection against early, postischemic oxidative stress.  

Physiologic Progesterone Reduces Mitochondrial Dysfunction And Hippocampal Cell Loss After Traumatic Brain Injury In Female Rats

Representative photomicrographs at high-powered magnification of the CA1 subfield of the hippocampus stained for NeuN from ipsilateral hemispheres in blank treated (A,B) and low range progesterone treated (C) at 7 days after TBI. In Figure 3A, a blank-implanted rat shows a marked reduction in total hippocampal neurons seen with NeuN labeling, with many abnormally stained neurons (arrow heads in inset) and few normally stained neurons (arrow in inset) amongst remaining cells. In Figure 3B, a blank-implanted rat shows a normal cell density, but an abundance of abnormally stained neurons (arrow heads in inset). Figure 3C shows a progesterone treated rat with preservation of normal cell numbers and a
predominance of normal NeuN staining (arrows in inset).