{"id":{"repo_id":"wfu","oai_identifier":"oai:wakespace.lib.wfu.edu:10339/39139"},"canonical_url":"https://search.dev.ndltd.org/etd/wfu/oai:wakespace.lib.wfu.edu:10339/39139","repository":{"repo_id":"wfu","name":"Wake Forest University","base_url":"https://wakespace.lib.wfu.edu/oai/request"},"display":{"title":"RADIATION-INDUCED BRAIN INJURY: NOT JUST A MICROGLIA AND HIPPOCAMPUS STORY ANYMORE","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).","abstract_html":"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).","abstract_has_math":false,"creators":["Moore, Elizabeth Diana"],"institution":"Wake Forest University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2013,"date_issued":"2013","date_published":"2013","updated_at":"2026-07-27T22:01:39Z","subjects":["Angiotensin-(1-7)"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10339/39139","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Moore, Elizabeth Diana"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2014-01-15T09:35:35Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2015-01-15T09:30:08Z"]},{"key":"dc:date.issued","label":"Date","values":["2013"]},{"key":"dc:publisher","label":"Institution","values":["Wake Forest University"]},{"key":"dc:type","label":"Dc Type","values":["Dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Angiotensin-(1-7)"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10339/39139"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["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)."]},{"key":"dc:title","label":"Title","values":["RADIATION-INDUCED BRAIN INJURY: NOT JUST A MICROGLIA AND HIPPOCAMPUS STORY ANYMORE"]}]}],"canonical_facts":{"dc:creator":["Moore, Elizabeth Diana"],"dc:date.accessioned":["2014-01-15T09:35:35Z"],"dc:date.available":["2015-01-15T09:30:08Z"],"dc:date.issued":["2013"],"dc:description.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)."],"dc:identifier.uri":["http://hdl.handle.net/10339/39139"],"dc:language.iso":["en"],"dc:publisher":["Wake Forest University"],"dc:subject":["Angiotensin-(1-7)"],"dc:title":["RADIATION-INDUCED BRAIN INJURY: NOT JUST A MICROGLIA AND HIPPOCAMPUS STORY ANYMORE"],"dc:type":["Dissertation"]},"updated_at":"2026-07-27T22:01:39Z"}