Small ubiquitin-like modifier 2 (SUMO2) is critical for memory processes in mice.

We have successfully developed various rodent models of brain and spinal cord injuries in our lab, such as focal cerebral ischemia, global cerebral ischemia, head trauma, subarachnoid hemorrhage, intracerebral hemorrhage, spinal cord ischemia and compression injury. We also established cardiac arrest and hemorrhagic shock models for studying multiple organ dysfunction.  Our current studies focus on two projects. One is to examine the efficacy of catalytic antioxidant in treating cerebral ischemia and the other is to examine the efficacy of post-conditioning on outcome of subarachnoid hemorrhage induced cognitive dysfunction.

Current clinical research interests include clinical trials regarding adaptive or closed-loop deep brain stimulation with novel devices, cellular, and gene therapy in Parkinson disease. Additional trials have included gene therapy for Alzheimer's disease and sensory restoration for development of brain machine interfaces. Clinical treatments include deep brain stimulation, which is now a common procedure for treating Parkinson disease and tremor. Translational approaches include testing new devices and stimulation patterns in the operating room. Pre-clinical research interests focus on evaluation of cerebral perfusion and metabolism changes with stroke, aging and Alzheimer's disease, using both in vivo and in vitro approaches. These basic science interests include new approaches to cerebral blood flow enhancement with brain stimulation, optical imaging of the brain, cellular understanding of metabolism using direct substrate recordings (ie, oxygen, glucose, lactate, respirometry) and developing new methods to understand neurovascular coupling, analyzing complex interactions between neurons, astrocytes and blood vessels.  Further interests include changes in cerebral blood flow with stroke and enhanced recovery after stroke.

RESEARCH INTERESTS
Last Updated: 27 October 2020

My laboratory uses genetically-modified mice to study the roles that certain genes and gene products play in the presentation of abnormal neuroendocrine, neurological, and psychiatric responses. Traditionally, the identification of neuroendocrine dysfunction has involved biochemical analyses of hormonal responses, those for neurological disorders have relied upon behavioral and postmortem analyses, and those for psychiatric conditions have depended upon phenomenology.  The use of genetic technologies has allowed specific genes in selected cells and in neural pathways to be related to certain molecular, biochemical, cellular, physiological, and behavioral dysfunctions. As the Director of the Mouse Behavioral and Neuroendocrine Analysis Core Facility at Duke University (http://sites.duke.edu/mousebehavioralcore/), we have phenotyped many different lines of inbred and mutant mice for my own work as well as for investigators at Duke and at other research institutions. As a consequence, we have helped to develop many different mouse genetic models of neuroendocrine and neuropsychiatric illness. We are working also with academic medicinal chemists and/or certain pharmacological/biotechnological companies to identify novel compounds that will ameliorate abnormal responses in various mutant mouse models. Some of these preclinical studies have formed a basis for clinical trials in humans.