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      Systemic infection and inflammation in acute CNS injury and chronic neurodegeneration: underlying mechanisms.

      1 ,
      Neuroscience
      Elsevier BV

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          Abstract

          We have all at some time experienced the non-specific symptoms that arise from being ill following a systemic infection. These symptoms, such as fever, malaise, lethargy and loss of appetite are often referred to as "sickness behavior" and are a consequence of systemically produced pro-inflammatory mediators. These inflammatory mediators signal to the brain, leading to activation of microglial cells, which in turn, signal to neurons to induce adaptive metabolic and behavioral changes. In normal healthy persons this response is a normal part of our defense, to protect us from infection, to maintain homeostasis and causes no damage to neurons. However, in animals and patients with chronic neurodegenerative disease, multiple sclerosis, stroke and even during normal aging, systemic inflammation leads to inflammatory responses in the brain, an exaggeration of clinical symptoms and increased neuronal death. These observations imply that, as the population ages and the number of individuals with CNS disorders increases, relatively common systemic infections and inflammation will become significant risk factors for disease onset or progression. In this review we discuss the underlying mechanisms responsible for sickness behavior induced by systemic inflammation in the healthy brain and how they might be different in individuals with CNS pathology.

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          Author and article information

          Journal
          Neuroscience
          Neuroscience
          Elsevier BV
          0306-4522
          0306-4522
          Feb 06 2009
          : 158
          : 3
          Affiliations
          [1 ] CNS Inflammation Group, School of Biological Sciences, University of Southampton, Biomedical Sciences Building, Bassett Crescent East, Southampton SO16 7PX, UK. jt8@soton.ac.uk
          Article
          S0306-4522(08)01045-2
          10.1016/j.neuroscience.2008.07.031
          18706982
          71e2bb6e-27b2-4ace-8d45-500ffad12b14
          History

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