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Susan Knoblach
Associate Research Professor of Genomics and Precision Medicine
Associate Research Professor of Pediatrics (Secondary)

Office Phone: 202-884-6094
Email: Email
Department: Genomics and Precision Medicine

Education

  • BS, Pennsylvania State University, 1982
  • PhD, Indiana University, 1994

Biography

Additional Education

Georgetown University Medical School, Washington DC Post-Doc CNS   Injury

Bibliography

Link to pubmed publications: http://www.ncbi.nlm.nih.gov/pubmed/?term=knoblach+sm

  • De Biase A*, Knoblach SM*, Di Giovanni S*, Fan C, Molon A, Hoffman EP, Faden AI. Gene expression profiling of experimental traumatic spinal cord injury as a function of distance from impact site and injury severity. Physiol Genomics. 2005  Aug 11;22(3):368-81. Epub 2005 Jun 7. PubMed PMID: 15942019. *first authors
     
  • Knoblach SM, Huang X, VanGelderen J, Calva-Cerqueira D, Faden AI. Selective caspase activation may contribute to neurological dysfunction after experimental spinal cord trauma. J Neurosci Res. 2005 May 1;80(3):369-80. PubMed PMID:15795935.
     
  • Knoblach SM, Alroy DA, Nikolaeva M, Cernak I, Stoica BA, Faden AI. Caspase inhibitor z-DEVD-fmk attenuates calpain and necrotic cell death in vitro and after traumatic brain injury. J Cereb Blood Flow Metab. 2004 Oct;24(10):1119-32. PubMed PMID: 15529012.
     
  • Faden AI, Knoblach SM, Cernak I, Fan L, Vink R, Araldi GL, Fricke ST, Roth BL, Kozikowski AP. Novel diketopiperazine enhances motor and cognitive recovery after traumatic brain injury in rats and shows neuroprotection in vitro and in vivo. J Cereb Blood Flow Metab. 2003 Mar;23(3):342-54. PubMed PMID: 12621309.
     
  • Di Giovanni S, Knoblach SM, Brandoli C, Aden SA, Hoffman EP, Faden AI. Gene profiling in spinal cord injury shows role of cell cycle in neuronal death. Ann Neurol. 2003 Apr;53(4):454-68. PubMed PMID: 12666113.
     
  • Allen JW, Knoblach SM, Faden AI. Activation of group I metabotropic glutamate receptors reduces neuronal apoptosis but increases necrotic cell death in vitro. Cell Death Differ. 2000 May;7(5):470-6. PubMed PMID: 10800080.
     
  • Allen JW, Knoblach SM, Faden AI. Combined mechanical trauma and metabolic impairment in vitro induces NMDA receptor-dependent neuronal cell death and caspase-3-dependent apoptosis. FASEB J. 1999 Oct;13(13):1875-82. PubMed PMID:10506592.
     
  • Knoblach SM, Fan L, Faden AI. Early neuronal expression of tumor necrosis factor-alpha after experimental brain injury contributes to neurological impairment. J Neuroimmunol. 1999 Mar 1;95(1-2):115-25. PubMed PMID: 10229121.
     
  • Knoblach SM, Faden AI. Interleukin-10 improves outcome and alters proinflammatory cytokine expression after experimental traumatic brain injury.  Exp Neurol. 1998 Sep;153(1):143-51. PubMed PMID: 9743576.
     
  • Yakovlev AG, Knoblach SM, Fan L, Fox GB, Goodnight R, Faden AI. Activation of CPP32-like caspases contributes to neuronal apoptosis and neurological dysfunction after traumatic brain injury. J Neurosci. 1997 Oct 1;17(19):7415-24. PubMed PMID: 9295387.

Research

  • Molecular analysis of pathological mechanisms of neuronal cell death
     
  • Elucidation of global and pathway-driven changes in gene expression and signaling networks involved in cell death,  plasticity, and/or regeneration related to acute injury or chronic neurodegenerative disease
     
  • Utilization of in vitro and in vivo models of neuronal cell death or CNS injury to develop neuroprotective drugs and predictive systems-based models of injury responses and mechanisms
     
  • Investigation of potential mechanistic or etiological relationships between acute CNS injury and chronic neurodegenerative disease

Publications

View publications by this faculty member.

Industry Relationships and Collaborations

This faculty member (or a member of their immediate family) has reported a financial interest with the health care related companies listed below. These relations have been reported to the University and, when appropriate, management plans are in place to address potential conflicts.

  • None