{"id":{"repo_id":"vt","oai_identifier":"oai:vtechworks.lib.vt.edu:10919/115429"},"canonical_url":"https://search.dev.ndltd.org/etd/vt/oai:vtechworks.lib.vt.edu:10919/115429","repository":{"repo_id":"vt","name":"Virginia Tech","base_url":"https://vtechworks.lib.vt.edu/oai/request"},"display":{"title":"Novel Diagnostic Approaches for Genetic and Environmental Sources of Mitochondrial Dysfunction","abstract":"With cardiovascular disease, diabetes mellitus, and neurodegenerative conditions on the rise, understanding their pathogenesis is paramount to tackling this public health crisis. Current research indicates that the primary cause of these diseases is mitochondrial dysfunction in the affected patients. While genetics plays a role in these conditions, lifestyle choices and exposure to toxins also significantly contribute to their development. Unfortunately, early-stage diagnosis can be difficult due to overlapping symptoms with other diseases. Developing innovative therapies that can prevent or reverse the deterioration of metabolic dysfunctions is critical to establishing early intervention. My research focused on investigating molecular targets linked with Friedrich's Ataxia, an inherited metabolic disorder, through conducting functional in-vitro studies using human-derived cell samples, as well as developing inventive animal models created via Xenopus laevis tadpoles to evaluate the effects of environmental stressors. My investigations have uncovered promising treatment options that improve mitochondrial function, mitigate oxidative stress, and elucidate critical mechanisms involved in environmentally induced disruptions to mitochondria.","abstract_html":"With cardiovascular disease, diabetes mellitus, and neurodegenerative conditions on the rise, understanding their pathogenesis is paramount to tackling this public health crisis. Current research indicates that the primary cause of these diseases is mitochondrial dysfunction in the affected patients. While genetics plays a role in these conditions, lifestyle choices and exposure to toxins also significantly contribute to their development. Unfortunately, early-stage diagnosis can be difficult due to overlapping symptoms with other diseases. Developing innovative therapies that can prevent or reverse the deterioration of metabolic dysfunctions is critical to establishing early intervention. My research focused on investigating molecular targets linked with Friedrich's Ataxia, an inherited metabolic disorder, through conducting functional in-vitro studies using human-derived cell samples, as well as developing inventive animal models created via Xenopus laevis tadpoles to evaluate the effects of environmental stressors. My investigations have uncovered promising treatment options that improve mitochondrial function, mitigate oxidative stress, and elucidate critical mechanisms involved in environmentally induced disruptions to mitochondria.","abstract_has_math":false,"creators":["Thomson, Alexander Hugh"],"institution":"Virginia Tech","degree_name":"Doctor of Philosophy","degree_level":"doctoral","degree_discipline":"Human Nutrition, Foods, and Exercise","degree_department":"Human Nutrition, Foods and Exercise","school":null,"contributors":[],"advisors":[],"committee_chairs":["Drake, Joshua Chadwick"],"committee_members":["Good, Deborah J.","Thompson, Christopher","Grange, Robert W."],"year":2023,"date_issued":"2023-06-14","date_published":"2023-06-14","updated_at":"2026-07-22T22:19:57Z","subjects":["mitochondria","metabolic diseases","Friedreich's ataxia","environmental toxins","developmental","Triclosan","treatments"],"languages":["en"],"rights":["Creative Commons Attribution 4.0 International"],"rights_urls":["http://creativecommons.org/licenses/by/4.0/"],"identifier_entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["vt_gsexam:37969"],"render_values":[{"text":"vt_gsexam:37969","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/10919/115429","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.committeechair","label":"Committee Chair","values":["Drake, Joshua Chadwick"]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["Good, Deborah J.","Thompson, Christopher","Grange, Robert W."]},{"key":"dc:contributor.department","label":"Department","values":["Human Nutrition, Foods and Exercise"]},{"key":"dc:creator","label":"Author","values":["Thomson, Alexander Hugh"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2023-06-15T08:00:27Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2023-06-15T08:00:27Z"]},{"key":"dc:date.issued","label":"Date","values":["2023-06-14"]},{"key":"dc:publisher","label":"Institution","values":["Virginia Tech"]},{"key":"dc:type","label":"Dc Type","values":["Dissertation"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Human Nutrition, Foods, and Exercise"]},{"key":"thesis:degree_level","label":"Degree Level","values":["doctoral"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Doctor of Philosophy"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["Virginia Polytechnic Institute and State University"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["mitochondria","metabolic diseases","Friedreich's ataxia","environmental toxins","developmental","Triclosan","treatments"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["Creative Commons Attribution 4.0 International"]},{"key":"dc:rights.uri","label":"Rights URI","values":["http://creativecommons.org/licenses/by/4.0/"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["vt_gsexam:37969"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10919/115429"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["With cardiovascular disease, diabetes mellitus, and neurodegenerative conditions on the rise, understanding their pathogenesis is paramount to tackling this public health crisis. Current research indicates that the primary cause of these diseases is mitochondrial dysfunction in the affected patients. While genetics plays a role in these conditions, lifestyle choices and exposure to toxins also significantly contribute to their development. Unfortunately, early-stage diagnosis can be difficult due to overlapping symptoms with other diseases. Developing innovative therapies that can prevent or reverse the deterioration of metabolic dysfunctions is critical to establishing early intervention. My research focused on investigating molecular targets linked with Friedrich's Ataxia, an inherited metabolic disorder, through conducting functional in-vitro studies using human-derived cell samples, as well as developing inventive animal models created via Xenopus laevis tadpoles to evaluate the effects of environmental stressors. My investigations have uncovered promising treatment options that improve mitochondrial function, mitigate oxidative stress, and elucidate critical mechanisms involved in environmentally induced disruptions to mitochondria."]},{"key":"dc:description.abstractgeneral","label":"General Abstract","values":["Metabolic dysfunction is a widespread health issue that affects millions of individuals each day. Its associated disorders, such as cardiovascular disease, diabetes, and neurodegenerative conditions, are rising due to various factors ranging from genetic predispositions to environmental and lifestyle-related risks. Therefore, there's an urgent need to identify this disorder early on and develop innovative treatment options. Considering this growing public health concern, it has become imperative to establish new methods for detecting metabolic dysfunction at its nascent stage while also exploring potential therapeutic interventions. Our research utilized cells derived from affected patients and animal models in devising novel approaches toward understanding the molecular mechanisms underpinning metabolic dysfunction. Our findings revealed several pathways and molecular targets contributing significantly to this condition, which could effectively be leveraged to develop targeted therapeutic strategies to combat its effects. Expanding our knowledge base will enable us to stay updated with emerging insights on treating metabolic dysfunction effectively while substantially improving patient outcomes."]},{"key":"dc:description.degree","label":"Dc Description Degree","values":["Doctor of Philosophy"]},{"key":"dc:format.medium","label":"Dc Format Medium","values":["ETD"]},{"key":"dc:title","label":"Title","values":["Novel Diagnostic Approaches for Genetic and Environmental Sources of Mitochondrial Dysfunction"]}]}],"canonical_facts":{"dc:contributor.committeechair":["Drake, Joshua Chadwick"],"dc:contributor.committeemember":["Good, Deborah J.","Thompson, Christopher","Grange, Robert W."],"dc:contributor.department":["Human Nutrition, Foods and Exercise"],"dc:creator":["Thomson, Alexander Hugh"],"dc:date.accessioned":["2023-06-15T08:00:27Z"],"dc:date.available":["2023-06-15T08:00:27Z"],"dc:date.issued":["2023-06-14"],"dc:description.abstract":["With cardiovascular disease, diabetes mellitus, and neurodegenerative conditions on the rise, understanding their pathogenesis is paramount to tackling this public health crisis. Current research indicates that the primary cause of these diseases is mitochondrial dysfunction in the affected patients. While genetics plays a role in these conditions, lifestyle choices and exposure to toxins also significantly contribute to their development. Unfortunately, early-stage diagnosis can be difficult due to overlapping symptoms with other diseases. Developing innovative therapies that can prevent or reverse the deterioration of metabolic dysfunctions is critical to establishing early intervention. My research focused on investigating molecular targets linked with Friedrich's Ataxia, an inherited metabolic disorder, through conducting functional in-vitro studies using human-derived cell samples, as well as developing inventive animal models created via Xenopus laevis tadpoles to evaluate the effects of environmental stressors. My investigations have uncovered promising treatment options that improve mitochondrial function, mitigate oxidative stress, and elucidate critical mechanisms involved in environmentally induced disruptions to mitochondria."],"dc:description.abstractgeneral":["Metabolic dysfunction is a widespread health issue that affects millions of individuals each day. Its associated disorders, such as cardiovascular disease, diabetes, and neurodegenerative conditions, are rising due to various factors ranging from genetic predispositions to environmental and lifestyle-related risks. Therefore, there's an urgent need to identify this disorder early on and develop innovative treatment options. Considering this growing public health concern, it has become imperative to establish new methods for detecting metabolic dysfunction at its nascent stage while also exploring potential therapeutic interventions. Our research utilized cells derived from affected patients and animal models in devising novel approaches toward understanding the molecular mechanisms underpinning metabolic dysfunction. Our findings revealed several pathways and molecular targets contributing significantly to this condition, which could effectively be leveraged to develop targeted therapeutic strategies to combat its effects. Expanding our knowledge base will enable us to stay updated with emerging insights on treating metabolic dysfunction effectively while substantially improving patient outcomes."],"dc:description.degree":["Doctor of Philosophy"],"dc:format.medium":["ETD"],"dc:identifier.other":["vt_gsexam:37969"],"dc:identifier.uri":["http://hdl.handle.net/10919/115429"],"dc:language.iso":["en"],"dc:publisher":["Virginia Tech"],"dc:rights":["Creative Commons Attribution 4.0 International"],"dc:rights.uri":["http://creativecommons.org/licenses/by/4.0/"],"dc:subject":["mitochondria","metabolic diseases","Friedreich's ataxia","environmental toxins","developmental","Triclosan","treatments"],"dc:title":["Novel Diagnostic Approaches for Genetic and Environmental Sources of Mitochondrial Dysfunction"],"dc:type":["Dissertation"],"thesis:degree_discipline":["Human Nutrition, Foods, and Exercise"],"thesis:degree_level":["doctoral"],"thesis:degree_name":["Doctor of Philosophy"],"thesis:institution_name":["Virginia Polytechnic Institute and State University"]},"updated_at":"2026-07-22T22:19:57Z"}