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B. Medicine, 1986
Ph.D. Neuroscience, 1991

Position: Associate Professor

Department: Psychiatry

Email:    email address

Office: (604) 875-2000 ext 4726
Fax: (604) 875-3871

Research Description:

My research is on the mechanism of action of mood stabilizing drugs at molecular and cellular levels, with focus on the neuroprotective effects of these drugs against oxidative stress. Previously,we found that mood stabilizing drugs prevented oxidative damage and upregulated glutathione (GSH)/glutathione S-transferase (GST) detoxification pathway. My research objective is to understand the role of GSH/GST pathway in the pharmacological treatment of mood stabilizing drugs. Research aims are: 1) to examine if GSH and GST mediate the neuroprotective effects of mood stabilizing drugs against oxidative damage; 2) to determine the role of Nrf2 transcription factor in GSH/GST pathway regulated by mood stabilizing drugs; 3) to identify oxidative modifications of synaptic proteins and 4) to determine role of GSH/GST pathway in mood stabilizing treatment using animal models for depression and mania. This study will lead to identifying new therapeutic targets in the GSH/GST pathway for investigation in clinical trials in the near future, contributing to new and more effective therapies for bipolar disorder with fewer side effects.

Research techniques employed in my work include cell culturing, measurement of lipid peroxidation and protein oxidation, TUNEL staining, real time-PCR,DNA cloning, in vitro transcription and translation, cell transfection,immunoblotting analysis, co-immunoprecipitation, immunohistochemistry, electrophoretic mobility shift assay, locomotor activity analysis and forced swim test among others.

Selected References:

  1. Andreazza AC, Shao L, Wang JF and Young LT (2010). Decreased mitochondrial complex I activity and increased oxidative damage to mitochondrial proteins in the prefrontal cortex of patients with bipolar disorder. Archives of General Psychiatry, 67: 360-8.
  2. Gawryluk JW, Wang JF, Andreazza AC, Shao L, Young LT. (2010) Decreased levels of glutathione, the major brain antioxidant, in post-mortem prefrontal cortex from patients with psychiatric disorders. Int J Neuropsychopharmacol. 16: 1-8.
  3. Wang JF, Shao L, Sun X and Young LT (2009). Increased oxidative stress in anterior cingulate cortex of subjects with bipolar disorder and schizophrenia. Bipolar disorders, 11: 523-529
  4. Shao L, Cui J, Young LT and Wang JF (2008). The effect of mood stabilizer lithium on expression and activity of glutathione-S-transferase isoenzymes. Neuroscience, 151: 518-24.
  5. Wang JF (2007). Defects of mitochondrial electron transport chain in bipolar disorder: implications for mood stabilizing treatment. Canadian Journal of Psychiatry,52: 753-62. (Review)
  6. Cui J, Shao L, Young LT and Wang JF (2007). Role of glutathione in neuroprotective effects of mood stabilizing drugs lithium and valproate. Neuroscience, 144: 1447-53.
  7. Shao L, Sun X, Xu L, Young LT and Wang JF (2006). Mood stabilizing drug lithium increases expression of endoplasmic reticulum stress proteins in primary cultured rat cerebralcortical cells. Life Science, 78: 1317-23.
  8. Sun X, Wang JF, Tseng M and Young LT (2006). Down regulation in components of mitochondrial electron transport chain in post-mortem frontal cortex from subjects with bipolar disorder. Journal of Psychiatry and Neuroscience, 31: 189-96.
  9. Shao L, Young LT and Wang JF (2005). Chronic treatment with mood stabilizers lithium and valproate prevents excitotoxicity by inhibiting oxidative stress in rat cerebral cortical cells. Biological Psychiatry, 58: 879-84.
  10. Wang JF, Shao L, Sun X, Young LT (2004). Glutathione S-transferase is a novel target for mood stabilizing drugs in primary cultured neurons. Journal of Neurochemistry. 88: 1477-84.



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