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The effects of glucose-induced metabolic injury on microglia activity and survival

  • Author / Creator
    Kenawy, Sara M
  • Glucose is the sole fuel for the brain in normal physiological conditions. Absence of glucose or its presence in high concentrations has been shown to be harmful to neurons. Microglia, the innate immune cells of the brain, are the first line of defense against changes in the CNS environment and their activity influences neuronal survival to a great extent. The effects of glucose-induced metabolic injury on microglia are unclear. Thus, the aim of this study was to investigate how hyperglycemia and hypoglycemia affect microglial phagocytotic activity, survival and secretory profile. Results showed that glucose concentration significantly affected microglia release of pro-inflammatory cytokines and growth factors. Microglia phagocytic activity was decreased at high and low glucose concentrations as compared to normal. Interestingly, microglia deprived of glucose showed better survival, exhibited increased ramification and a more quiescent phenotype where microglia released significantly less pro-inflammatory cytokines and growth factors as compared to controls

  • Subjects / Keywords
  • Graduation date
    2013-06
  • Type of Item
    Thesis
  • Degree
    Master of Science
  • DOI
    https://doi.org/10.7939/R3T12D
  • License
    This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for non-commercial purposes. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.
  • Language
    English
  • Institution
    University of Alberta
  • Degree level
    Master's
  • Department
    • Centre for Neuroscience
  • Supervisor / co-supervisor and their department(s)
    • Kathryn G Todd (Centre for Neurosciences)
  • Examining committee members and their departments
    • Ian winship (Centre for Neurosciences)
    • Glenn Baker (Centre for Neurosciences)
    • Kathryn G Todd (Centre for Neurosciences)
    • Kerr Bradely (Pharmacology)