Bookmark and Share

Personnel

Director

Dr. Faden
 

Alan I. Faden, M.D.
Director, Center for Shock, Trauma & Anesthesiology Research (STAR)
David S. Brown Professor in Trauma in the Department of Anesthesiology
 

Our laboratory uses multi-disciplinary approaches including molecular and cellular biology, animal modeling, behavior, imaging and drug discovery- to examine the pathobiology of experimental brain and spinal cord injury and their treatment. Specific research focuses include cell cycle pathways, microglial activation, cell death mechanisms, metabotropic glutamate receptors, and development of combination and multifunctional drug treatment strategies for neurotrauma.


 

Faculty

Dr. Stoica
 

Bogdan Stoica, M.D.
Assistant Professor of Anesthesiology 

Studies various neuronal cell death mediators, including cell cycle proteins, ceramide, endocannabinoids, BH3 domain pro-apoptotic factors and PARP. He also examines the protective effects of cyclin-dependent kinase inhibitors, as well as caspase inhibitors, in multiple in vitro and in vivo models.


 
David Loane
 

David J. Loane, Ph.D.
Assistant Professor of Anesthesiology 

Studies the pathophysiological role of beta amyloid in brain trauma, as well as a protective role for secretase inhibition. Also examines role of microglial associated inflammation in chronic and age-related neurodegeneration and therapeutic strategies that inhibit microglial-mediated neuroinflammation. Experimental approaches include rodent models of TBI, cell and molecular biology, behavioral testing, MRI imaging and quantitative histology.


 
Dr. Wu
 

Junfang Wu, B.M., Ph.D.
Assistant Professor 

Examines secondary injury processes following traumatic spinal cord injury (SCI) and pharmacological/gene therapeutic interventions for SCI. More specifically, studies the pathophysiological role of cell cycle activation in SCI using complementary genetic and pharmacological strategies. Also studies nocifensive behaviors and central pain regulation after experimental SCI, and the role of mitochondrial DNA in cell death.


 
marta 
 

Marta Lipinski, Ph.D.
Assistant Professor 

Autophagy, a catabolic process mediating the turnover of bulk cytoplasmic constituents including organelles and protein aggregates in a lysosome-dependent manner, protects organisms from a variety of diseases, including neurodegeneration, cancer and aging. Up-regulation of autophagy has also been observed following traumatic brain injury (TBI), but its function in this context remains unknown. My lab uses in vivo and in vitro models to examine the role of autophagy after traumatic injury, and to delineate the molecular mechanisms involved. Since mitochondrial damage plays an important role in neurodegeneration associated with both TBI and Parkinson’s disease (PD), and prior head injury is a well-established epidemiological factor for PD, we are also examining the potential role in TBI of genes known to be involved in the regulation of mitochondrial autophagy (mitophagy) in PD. Our long-term goal is to define novel druggable target molecules and pathways for the effective modulation of autophagy in TBI and other neurodegenerative diseases.


 
Fengtian Xue
 

Fengtian Xue, Ph.D.
Assistant Professor 

Synthesizes novel small molecules that activate the metabotropic glutamate receptor 5 (mGluR5) as potential treatment for human traumatic brain injury (TBI). He develops novel agonists of mGluR5 using structure-based drug design in combination of medicinal chemistry by targeting the extracellular ligand binding region (LBR) of the receptor. He also synthesizes novel positive allosteric modulators (PAMs) of mGluR5 by targeting the 7-helical transmembrane domain (7-TM) of mGluR5.


 
Shruti Kabadi
 

Shruti V. Kabadi, Ph.D.
Research Associate 

Research interests involve investigation of neurobehavioral (sensorimotor, cognition, anxiety and depression) dysfunction induced by traumatic brain injury (TBI) using multiple models of brain trauma on rats and mice, and evaluation of potential therapeutic strategies. The focus of my research is understanding the correlation between TBI-induced functional deficits and underlying pathophysiological mechanisms such as neuronal cell loss and inflammation, particularly microglial and astrocytic activation.


 

Post Docs

  • Stephanie Aungst, Ph.D.
  • Alok Kumar, Ph.D.
  • Boris Sabirzhanov, Ph.D.
  • Chinmoy Sarkar, Ph.D.
  • Zaorui “Jerry” Zhao, Ph.D.

Doctoral Student

  • Jacob Skovira

LAB TECHNICIANS

  • Guanghui Li