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This version was published on June 1, 2008
The Neuroscientist, Vol. 14, No. 3, 235-239 (2008)
DOI: 10.1177/1073858407309544

Acute Hypoxia, Diabetes, and Neuroimmune Dysregulation: Converging Mechanisms in the Brain

Daniel R. Johnson

Department of Animal Sciences, Department of Pathology

Christina L. Sherry

Department of Pathology, Division of Nutritional Sciences (CLS, GGF), University of Illinois at Urbana-Champaign, Urbana, Illinois

Jason M. York

Department of Animal Sciences, Department of Pathology

Gregory G. Freund

Department of Animal Sciences, freun{at}uiuc.edu, Division of Nutritional Sciences (CLS, GGF), University of Illinois at Urbana-Champaign, Urbana, Illinois, Department of Pathology

Acute hypoxia is experienced by a variety of individuals (neonates to the elderly) and in an assortment of conditions and diseases (terrorist bomb attack to decompensated heart failure). Increasingly, elaboration of inflammatory cytokines appears key to the brain-based response to hypoxia, as evidenced by the biobehaviors of malaise, fatigue, lethargy, and loss of interest in the physical and social environment. These sickness symptoms implicate hypoxia-dependent activation of the neuroimmune system as a key component of acute hypoxia. Type 2 diabetes (T2D) is associated with increased incidence, severity, and delayed recovery from hypoxic events. Why T2D negatively affects acute hypoxia is not well understood. Recent work, however, reveals that anti-inflammatory pathways tied to the interleukin (IL)-1β arm of the neuroimmune system may be critical. In this review, the authors examine the link between acute hypoxia, T2D, and neuroimmunity. NEUROSCIENTIST 14(3):235–239, 2008. DOI: 10.1177/1073858407309544

Key Words: Acute hypoxia • Type 2 diabetes • Neuroimmunity


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