{"id":{"repo_id":"uwo","oai_identifier":"oai:uwo.scholaris.ca:20.500.14721/37299"},"canonical_url":"https://search.dev.ndltd.org/etd/uwo/oai:uwo.scholaris.ca:20.500.14721/37299","repository":{"repo_id":"uwo","name":"Western University","base_url":"https://uwo.scholaris.ca/server/oai/request"},"display":{"title":"Modelling Prenatal Hypoxia As A Risk Factor For Schizophrenia Vulnerability In Patient-Derived Cerebral Organoids","abstract":"Prenatal hypoxia during fetal development is a significant environmental risk factor linked to schizophrenia (SCZ) vulnerability. However, hypoxia’s impact on human brain development at the cellular level remains unclear. Our laboratory has developed human cerebral organoids using induced pluripotent stem cells (iPSCs) derived from healthy control or SCZ patient cell lines to address these questions. This creates a platform that allows for the investigation into the pathophysiology of SCZ and hypoxia in tandem. Organoids were exposed to hypoxic conditions at one month of development, mimicking the early stages of cortical growth in the human fetus. Results reveal innate differences in neuronal development markers in SCZ organoids at the transcriptomic and protein level. In response to hypoxia, SCZ organoids exhibit dysregulation of mitochondrial-associated proteins and genes required for normal metabolism and growth. Our findings highlight critical differences in the expression of vital neuronal markers in SCZ and highlight hypoxia’s further impacts on neurodevelopmental pathophysiology related to SCZ risk.","abstract_html":"Prenatal hypoxia during fetal development is a significant environmental risk factor linked to schizophrenia (SCZ) vulnerability. However, hypoxia’s impact on human brain development at the cellular level remains unclear. Our laboratory has developed human cerebral organoids using induced pluripotent stem cells (iPSCs) derived from healthy control or SCZ patient cell lines to address these questions. This creates a platform that allows for the investigation into the pathophysiology of SCZ and hypoxia in tandem. Organoids were exposed to hypoxic conditions at one month of development, mimicking the early stages of cortical growth in the human fetus. Results reveal innate differences in neuronal development markers in SCZ organoids at the transcriptomic and protein level. In response to hypoxia, SCZ organoids exhibit dysregulation of mitochondrial-associated proteins and genes required for normal metabolism and growth. Our findings highlight critical differences in the expression of vital neuronal markers in SCZ and highlight hypoxia’s further impacts on neurodevelopmental pathophysiology related to SCZ risk.","abstract_has_math":false,"creators":["Gummerson, Dana M"],"institution":"The University of Western Ontario","degree_name":"M Sc","degree_level":null,"degree_discipline":"Neuroscience","degree_department":null,"school":null,"contributors":[],"advisors":["Laviolette, Steven R"],"committee_chairs":[],"committee_members":[],"year":2023,"date_issued":"2023-09-13","date_published":"2023-09-13","updated_at":"2026-07-27T21:56:09Z","subjects":["Cerebral organoid","Schizophrenia","Hypoxia","Mitochondrial dysfunction","Fetal brain development"],"languages":["en_ca"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://hdl.handle.net/20.500.14721/37299","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Laviolette, Steven R"]},{"key":"dc:creator","label":"Author","values":["Gummerson, Dana M"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2025-07-10T21:33:13Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2025-07-10T21:33:13Z"]},{"key":"dc:date.issued","label":"Date","values":["2023-09-13"]},{"key":"dc:publisher","label":"Institution","values":["The University of Western Ontario"]},{"key":"dc:type","label":"Dc Type","values":["thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Neuroscience"]},{"key":"thesis:degree_name","label":"Degree Name","values":["M Sc"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Cerebral organoid","Schizophrenia","Hypoxia","Mitochondrial dysfunction","Fetal brain development"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en_ca"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://hdl.handle.net/20.500.14721/37299"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["The thesis cover page in the PDF document includes references to Western University’s previous institutional repository platform, known as Scholarship@Western, and links to that platform (beginning with ir.lib.uwo.ca). In citing or referring to this thesis, use the DOI or handle from this page instead. Sample citation: Author name, \"Thesis title.\" (Year). Western University Open Repository. https://doi.org/10.71858/123456."]},{"key":"dc:description.abstract","label":"Abstract","values":["Prenatal hypoxia during fetal development is a significant environmental risk factor linked to schizophrenia (SCZ) vulnerability. However, hypoxia’s impact on human brain development at the cellular level remains unclear. Our laboratory has developed human cerebral organoids using induced pluripotent stem cells (iPSCs) derived from healthy control or SCZ patient cell lines to address these questions. This creates a platform that allows for the investigation into the pathophysiology of SCZ and hypoxia in tandem. Organoids were exposed to hypoxic conditions at one month of development, mimicking the early stages of cortical growth in the human fetus. Results reveal innate differences in neuronal development markers in SCZ organoids at the transcriptomic and protein level. In response to hypoxia, SCZ organoids exhibit dysregulation of mitochondrial-associated proteins and genes required for normal metabolism and growth. Our findings highlight critical differences in the expression of vital neuronal markers in SCZ and highlight hypoxia’s further impacts on neurodevelopmental pathophysiology related to SCZ risk."]},{"key":"dc:title","label":"Title","values":["Modelling Prenatal Hypoxia As A Risk Factor For Schizophrenia Vulnerability In Patient-Derived Cerebral Organoids"]}]}],"canonical_facts":{"dc:contributor.advisor":["Laviolette, Steven R"],"dc:creator":["Gummerson, Dana M"],"dc:date.accessioned":["2025-07-10T21:33:13Z"],"dc:date.available":["2025-07-10T21:33:13Z"],"dc:date.issued":["2023-09-13"],"dc:description":["The thesis cover page in the PDF document includes references to Western University’s previous institutional repository platform, known as Scholarship@Western, and links to that platform (beginning with ir.lib.uwo.ca). In citing or referring to this thesis, use the DOI or handle from this page instead. Sample citation: Author name, \"Thesis title.\" (Year). Western University Open Repository. https://doi.org/10.71858/123456."],"dc:description.abstract":["Prenatal hypoxia during fetal development is a significant environmental risk factor linked to schizophrenia (SCZ) vulnerability. However, hypoxia’s impact on human brain development at the cellular level remains unclear. Our laboratory has developed human cerebral organoids using induced pluripotent stem cells (iPSCs) derived from healthy control or SCZ patient cell lines to address these questions. This creates a platform that allows for the investigation into the pathophysiology of SCZ and hypoxia in tandem. Organoids were exposed to hypoxic conditions at one month of development, mimicking the early stages of cortical growth in the human fetus. Results reveal innate differences in neuronal development markers in SCZ organoids at the transcriptomic and protein level. In response to hypoxia, SCZ organoids exhibit dysregulation of mitochondrial-associated proteins and genes required for normal metabolism and growth. Our findings highlight critical differences in the expression of vital neuronal markers in SCZ and highlight hypoxia’s further impacts on neurodevelopmental pathophysiology related to SCZ risk."],"dc:identifier.uri":["https://hdl.handle.net/20.500.14721/37299"],"dc:language.iso":["en_ca"],"dc:publisher":["The University of Western Ontario"],"dc:subject":["Cerebral organoid","Schizophrenia","Hypoxia","Mitochondrial dysfunction","Fetal brain development"],"dc:title":["Modelling Prenatal Hypoxia As A Risk Factor For Schizophrenia Vulnerability In Patient-Derived Cerebral Organoids"],"dc:type":["thesis"],"thesis:degree_discipline":["Neuroscience"],"thesis:degree_name":["M Sc"]},"updated_at":"2026-07-27T21:56:09Z"}