Gregory G Freund

Biography

He has done his M.D., 1988, Univ. of Rochester School of Medicine and Dentistry, New York, B.A., 1983, Wesleyan University, Middletown, Connecticut.

Research Interest

After receiving my BA in Studio Art from Wesleyan University, I went on to study medicine and pathology at the University of Rochester. At Rochester, I was fascinated by the emerging field of brain-immune communication especially as related to diabesity. There I performed formative work demonstrating that immune cells had functional insulin and IGF-1 receptor signaling systems. Currently, I am Professor and Head of Pathology at the University of Illinois at Urbana-Champaign examining the immune-associated biobehavioral complications of diabesity in mice. We are particularly focused on neuroimmune dysregulation and the development of countermeasures to protect against adverse cognitive function tied to oxidative stress and pro-inflammation. In this regard, we were the first to show that diabesity hindered recovery from lipopolysaccharide (LPS)- and IL-1-induced neuroinflammation (O'Connor JC, et al. 2005 J Immunol). We demonstrated that diabesity-associated IGF-1/insulin resistance could be overcome with the IGF-1/insulin mimetic, vanadyl sulfate, speeding recovery from LPS-induced neuroinflammation (Johnson DR, et al. 2005 Proc Natl Acad Sci). We discovered that the oxidative stressor hypoxia/reoxygenation activated the IL-1beta arm of the neuroimmune system via caspase-1 and that diabesity exacerbated the associated adverse behavioral outcomes (Johnson DR, et al. 2007 J Neurosci). Most recently we identified adenosine as a key danger signal responsible for hypoxia/reoxygenation-dependent activation of the inflammasome in the brain (Chiu GS, et al. 2012 J Neurosci). Coupled to our demonstration that metabolic stress impairs learning and memory in juvenile mice (Kaczmarczyk MM, et al. in press Psychoneuroendocrinology), we have begun to delineate a mechanism by which oxidative stress triggers the IL-1beta arm of the neuroimmune system and negatively impacts cognition.