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Andy P. Li, M.D., Ph.D.

Andy P. Li, M.D., Ph.D.
Andy P. Li, M.D., Ph.D., Chair, Department of Pharmaceutical Sciences
  • Earned M.D. at Ningxia Medical University, Beijing, China, 1982
  • Earned PhD in Neurobiology at the University of Lund, Sweden, 1996
  • Contact: pli@nccu.edu or 919-530-6872

Research Interests

Mechanism and Treatment of Brain Damage After Cerebral Stroke and Traumatic Brain Injury

The core focus of this research is cell death and survival pathways, free radicals, neuro-inflammation, astrocytic response and neuro-protection after stroke and TBI. The study seeks to determine validity of the hypothesis that cerebral stroke and TBI lead to neuron damage by increasing free radical production, enhancing neuro-inflammation, suppressing cell survival pathways and causing cell death of necrosis and/or apoptosis. It is believed that agents aimed at blocking these biochemical cascades could provide protection against stroke and TBI.

Exacerbation Effects of Hyperglycemia on Stroke and TBI

Core focus revolves around mechanisms by which hyperglycemia mellitus enhances ischemic and traumatic brain injuries. The research seeks to prove that 1) hyperglycemia enhances damage by causing early mitochondrial failure and 2) preservation of mitochondrial function reduces hyperglycemia enhanced damage.

Mitochondrial Biogenesis as a Therapeutic Strategy for Neurodegenerative Disorders

Using chemical and genetic approach to activate mitochondrial biogenesis and testing the efficacy of various compounds on in vitro models of Parkinson’s disease, hypoxia and glutamate toxicity.

Publications

  • Muranyi M, He QP, Fujioka M, Han A, Csiszar K, Li PA (2003) Diabetes activates cell death pathway after transient focal cerebral ischemia. Diabetes 52:481-486
  • Muranyi M, Ding C, He Q, Lin Y, Li PA. (2006) Streptozotocin-induced diabetes mellitus causes astrocyte damage after ischemia and reperfusion injury. Diabetes 55:349-355.
  • Mehta SL Li PA (2009) Neuroprotective role of mitochondrial uncoupling protein 2 in cerebral stroke. J Cereb blood Flow Metab, 29:1069-1078.
  • Haines B, Suresh Mehta, Pratt S, Warden C, Li PA (2010) Deletion of mitochondrial uncoupling protein-2 increases ischemic brain damage after transient focal ischemia by altering gene expression patterns and enhancing inflammatory cytokines. J. Cereb. Blood Flow Metab. 30:1825-33
  • Mendelev N, Mehta SL, Witherspoon S, He Q, Sexton JZ, Li PA (2011) Upregulation of Human Selenoprotein H in murine hippocampal neuronal cells promotes mitochondrial functional performance and biogenesis. Mitochondrion. 11:76-82.
  • Yi Ma, Suresh L. Mehta, Baisong Lu, P. Andy Li (2011) Deficiency in the inner mitochondrial membrane peptidase 2-like (Immp2l) gene increases ischemic brain damage and impairs mitochondrial function. Neurobiol Dis. 44:270-276.
  • Santosh Kumari, Suresh L. Mehta, P. Andy Li (2012). Glutamate induces mitochondrial dynamic imbalance and autophagy activation: preventive effects of selenium. PLoS One 7:e3982. Doi:101371/ journal.pone.0039382
  • Mehta Sl, Mendelev N, Kumari S, Li PA (2013). Overexpression of human selenoprotein H in neuronal cells enhances mitochondrial biogenesis and function through activation of protein kinase A, protein kinase B, and cyclic adenosine monophosphate response element-binding protein pathway. Int J Biochem Cell Biol 45:604-611
  • Jing L, Wang JG, Zhang JZ, Cao CX, Chang Y, Dong JD, Guo FY, Li PA. (2014) Upregulation of ICAM-1 in diabetic rats after transient forebrain ischemia and reperfusion injury. J Inflamm 11: 35-59.
  • Yang X, He C, Liu P Song Y, Thomas T, Tshimanga S, Wang F, Niu JG, Sun T, Li PA (2015). Inhibition of mTOR Pathway by Rapamycin Reduces Brain Damage in Rats Subjected to Transient Forebrain Ischemia. Int J Biol Sci 11:1424-1435.
 
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