2026-09-24T11:33:09Zhttps://wakespace.lib.wfu.edu/server/oai/request

oai:null:10339/391392026-09-18T14:15:12Zcom_10339_14934col_10339_38132

Moore, Elizabeth Diana 2014-01-15T09:35:35Z 2015-01-15T09:30:08Z 2013 https://wakespace.lib.wfu.edu/handle/10339/39139 As the population of long-term cancer survivors increases, quality of life (QOL) is becoming an important aspect of cancer therapy. The majority of brain tumor patients surviving 6 months after fractionated whole brain irradiation (fWBI) will develop progressive, irreversible cognitive impairment that has a significant effect on their QOL. Although the mechanism(s) behind the development of radiation-induced brain injury, including cognitive impairment, are unknown, hippocampal microglia-mediated neuroinflammation and altered neuronal function are hypothesized to play a role. However, cognitive studies with renin-angiotensin system (RAS) blockers which increase Ang-(1-7), indicate that microglia and the hippocampus may not be the complete story. Thus, we hypothesized that radiation-induced brain injury may be prevented by i] targeting neuroinflammation in brain cells other than microglia, and by ii] altering neuronal function in other brain regions (e.g. cortex). en Wake Forest University Angiotensin-(1-7) Brain Cognition Homer1a Radiation RADIATION-INDUCED BRAIN INJURY: NOT JUST A MICROGLIA AND HIPPOCAMPUS STORY ANYMORE Dissertation Metheny-Barlow, Linda J Gallagher, Patricia Blackstock, William Miller, Lance Seals, Darren Riddle, David Cancer Biology 2015-01-15 open.access