Item Details

abstract

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).

subject

Angiotensin-(1-7)

Brain

Cognition

Homer1a

Radiation

contributor

Moore, Elizabeth Diana (author)

Metheny-Barlow, Linda J (committee chair)

Gallagher, Patricia (committee member)

Blackstock, William (committee member)

Miller, Lance (committee member)

Seals, Darren (committee member)

Riddle, David (committee member)

date

2014-01-15T09:35:35Z (accessioned)

2015-01-15T09:30:08Z (available)

2013 (issued)

degree

Cancer Biology (discipline)

embargo

2015-01-15 (terms)

identifier

http://hdl.handle.net/10339/39139 (uri)

language

en (iso)

publisher

Wake Forest University

title

RADIATION-INDUCED BRAIN INJURY: NOT JUST A MICROGLIA AND HIPPOCAMPUS STORY ANYMORE

type

Dissertation