{"id":{"repo_id":"calgary","oai_identifier":"oai:ucalgary.scholaris.ca:1880/123616"},"canonical_url":"https://search.dev.ndltd.org/etd/calgary/oai:ucalgary.scholaris.ca:1880/123616","repository":{"repo_id":"calgary","name":"University of Calgary","base_url":"https://ucalgary.scholaris.ca/server/oai/request"},"display":{"title":"Exploring Neural Activities in the Prefrontal Cortex of Fragile X Syndrome Mouse Models Using Electroencephalography","abstract":"Fragile X syndrome (FXS) is the most common inherited cause of intellectual disability and a leading monogenic contributor to autism spectrum disorder. Human EEG studies have identified alterations in gamma power, alpha slowing, cross-frequency coupling, and reduced signal complexity, suggesting potential translational biomarkers of network dysfunction. However, the extent to which these signatures are conserved in preclinical models—especially in female mice—remains unclear. This thesis aimed to characterize oscillatory alterations in female Fmr1 knockout (KO) mice on a C57BL/6J background and to evaluate whether EEG-derived metrics align with human findings. Analyses of spectral power, peak alpha frequency, theta–beta ratio, cross-frequency coupling, and signal complexity revealed reduced alpha power, slowed peak alpha frequency, disrupted coupling, and altered gamma activity. These features partially mirror abnormalities reported in FXS patients, underscoring EEG’s translational relevance. By extending analysis beyond traditional spectral power, this work establishes a bridge between preclinical and clinical EEG metrics and highlights the importance of including female models to advance biomarker development and translational research in FXS.","abstract_html":"Fragile X syndrome (FXS) is the most common inherited cause of intellectual disability and a leading monogenic contributor to autism spectrum disorder. Human EEG studies have identified alterations in gamma power, alpha slowing, cross-frequency coupling, and reduced signal complexity, suggesting potential translational biomarkers of network dysfunction. However, the extent to which these signatures are conserved in preclinical models—especially in female mice—remains unclear. This thesis aimed to characterize oscillatory alterations in female Fmr1 knockout (KO) mice on a C57BL/6J background and to evaluate whether EEG-derived metrics align with human findings. Analyses of spectral power, peak alpha frequency, theta–beta ratio, cross-frequency coupling, and signal complexity revealed reduced alpha power, slowed peak alpha frequency, disrupted coupling, and altered gamma activity. These features partially mirror abnormalities reported in FXS patients, underscoring EEG’s translational relevance. By extending analysis beyond traditional spectral power, this work establishes a bridge between preclinical and clinical EEG metrics and highlights the importance of including female models to advance biomarker development and translational research in FXS.","abstract_has_math":false,"creators":["Wang, Bosong"],"institution":"Cumming School of Medicine","degree_name":"Master of Science (MSc)","degree_level":null,"degree_discipline":"Medicine – Neuroscience","degree_department":null,"school":null,"contributors":[],"advisors":["Cheng, Ning","Yan, Jun"],"committee_chairs":[],"committee_members":["Whelan, Patrick","Bray, Signe","Yang, Guang"],"year":2025,"date_issued":"2025-12-18","date_published":"2025-12-18","updated_at":"2026-07-24T01:30:18Z","subjects":["Fragile X syndrome","Female","Mouse model","Electroencephalography","Juvenile mice","C57BL/6J","Thalamocortical network"],"languages":["en"],"rights":["Unless otherwise indicated, this material is protected by copyright and has been made available with authorization from the copyright owner. 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However, the extent to which these signatures are conserved in preclinical models—especially in female mice—remains unclear. This thesis aimed to characterize oscillatory alterations in female Fmr1 knockout (KO) mice on a C57BL/6J background and to evaluate whether EEG-derived metrics align with human findings. Analyses of spectral power, peak alpha frequency, theta–beta ratio, cross-frequency coupling, and signal complexity revealed reduced alpha power, slowed peak alpha frequency, disrupted coupling, and altered gamma activity. These features partially mirror abnormalities reported in FXS patients, underscoring EEG’s translational relevance. By extending analysis beyond traditional spectral power, this work establishes a bridge between preclinical and clinical EEG metrics and highlights the importance of including female models to advance biomarker development and translational research in FXS."]},{"key":"dc:title","label":"Title","values":["Exploring Neural Activities in the Prefrontal Cortex of Fragile X Syndrome Mouse Models Using Electroencephalography"]}]}],"canonical_facts":{"dc:contributor.advisor":["Cheng, Ning","Yan, Jun"],"dc:contributor.committeemember":["Whelan, Patrick","Bray, Signe","Yang, Guang"],"dc:creator":["Wang, Bosong"],"dc:date":["2026-06"],"dc:date.accessioned":["2025-12-22T16:00:27Z"],"dc:date.issued":["2025-12-18"],"dc:description.abstract":["Fragile X syndrome (FXS) is the most common inherited cause of intellectual disability and a leading monogenic contributor to autism spectrum disorder. 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