The FDA-approved amyotrophic lateral sclerosis (ALS) drug Riluzole has great potential in treating Alzheimer’s disease (AD) based on promising animal data as well as its known action on modulating synaptic transmission. However, its detailed mechanism of action is not fully understood. Here, we proposed work aiming to address this aspect via focus- ing on the Heat Shock Factor 1 (HSF1)-dependent mechanisms. We found that Riluzole could increase HSF1 and BDNF (Brain-Derived Neurotrophic Factor) expression both at transcriptional and translational levels. CA1 (Cornu Ammonia, the first region in the hip- pocampal circuit), is its main target. We also demonstrated a protective role of Riluzole on rat primary neuronal culture which was abolished by a HSF1 inhibitor. Current data together suggest that Riluzole’s synaptic-protective mechanism is highly possible through a HSF1-BDNF axis. The positive outcome from this study will facilitate filling our knowl- edge gap and interpretation of the ongoing clinical trials of Riluzole in AD in which the final data will be released later this year.
","abstract_html":"<p>The FDA-approved amyotrophic lateral sclerosis (ALS) drug Riluzole has great potential in treating Alzheimer’s disease (AD) based on promising animal data as well as its known action on modulating synaptic transmission. However, its detailed mechanism of action is not fully understood. Here, we proposed work aiming to address this aspect via focus- ing on the Heat Shock Factor 1 (HSF1)-dependent mechanisms. We found that Riluzole could increase HSF1 and BDNF (Brain-Derived Neurotrophic Factor) expression both at transcriptional and translational levels. CA1 (Cornu Ammonia, the first region in the hip- pocampal circuit), is its main target. We also demonstrated a protective role of Riluzole on rat primary neuronal culture which was abolished by a HSF1 inhibitor. Current data together suggest that Riluzole’s synaptic-protective mechanism is highly possible through a HSF1-BDNF axis. The positive outcome from this study will facilitate filling our knowl- edge gap and interpretation of the ongoing clinical trials of Riluzole in AD in which the final data will be released later this year.</p>","abstract_has_math":false,"creators":["Zhang, Yi"],"institution":null,"degree_name":"Master of Science (MS)","degree_level":"Thesis","degree_discipline":"Biomedical Sciences","degree_department":null,"school":null,"contributors":["Liao, Francesca-Fang"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019-08-01T07:00:00Z","date_published":"2019-08-01T07:00:00Z","updated_at":"2026-07-24T05:00:33Z","subjects":["Hippocampus","HSF-BDNF Axis","Molecular Mechanism","Neuroscience","Pharmacology","Riluzole","Medicine and Health Sciences"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://dc.uthsc.edu/dissertations/497","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Liao, Francesca-Fang"]},{"key":"dc:creator","label":"Author","values":["Zhang, Yi"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2019-10-24T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biomedical Sciences"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (MS)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Hippocampus","HSF-BDNF Axis","Molecular Mechanism","Neuroscience","Pharmacology","Riluzole","Medicine and Health Sciences"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://dc.uthsc.edu/dissertations/497"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["The FDA-approved amyotrophic lateral sclerosis (ALS) drug Riluzole has great potential in treating Alzheimer’s disease (AD) based on promising animal data as well as its known action on modulating synaptic transmission. However, its detailed mechanism of action is not fully understood. Here, we proposed work aiming to address this aspect via focus- ing on the Heat Shock Factor 1 (HSF1)-dependent mechanisms. We found that Riluzole could increase HSF1 and BDNF (Brain-Derived Neurotrophic Factor) expression both at transcriptional and translational levels. CA1 (Cornu Ammonia, the first region in the hip- pocampal circuit), is its main target. We also demonstrated a protective role of Riluzole on rat primary neuronal culture which was abolished by a HSF1 inhibitor. Current data together suggest that Riluzole’s synaptic-protective mechanism is highly possible through a HSF1-BDNF axis. The positive outcome from this study will facilitate filling our knowl- edge gap and interpretation of the ongoing clinical trials of Riluzole in AD in which the final data will be released later this year.
"]},{"key":"dc:title","label":"Title","values":["Investigation of Riluzole’s Synaptic Protection Mechanism Through HSF1-BDNF Axis"]}]}],"canonical_facts":{"dc:contributor":["Liao, Francesca-Fang"],"dc:creator":["Zhang, Yi"],"dc:date.available":["2019-10-24T07:00:00Z"],"dc:description.abstract":["The FDA-approved amyotrophic lateral sclerosis (ALS) drug Riluzole has great potential in treating Alzheimer’s disease (AD) based on promising animal data as well as its known action on modulating synaptic transmission. However, its detailed mechanism of action is not fully understood. Here, we proposed work aiming to address this aspect via focus- ing on the Heat Shock Factor 1 (HSF1)-dependent mechanisms. We found that Riluzole could increase HSF1 and BDNF (Brain-Derived Neurotrophic Factor) expression both at transcriptional and translational levels. CA1 (Cornu Ammonia, the first region in the hip- pocampal circuit), is its main target. We also demonstrated a protective role of Riluzole on rat primary neuronal culture which was abolished by a HSF1 inhibitor. Current data together suggest that Riluzole’s synaptic-protective mechanism is highly possible through a HSF1-BDNF axis. The positive outcome from this study will facilitate filling our knowl- edge gap and interpretation of the ongoing clinical trials of Riluzole in AD in which the final data will be released later this year.
"],"dc:identifier":["https://dc.uthsc.edu/dissertations/497"],"dc:subject":["Hippocampus","HSF-BDNF Axis","Molecular Mechanism","Neuroscience","Pharmacology","Riluzole","Medicine and Health Sciences"],"dc:title":["Investigation of Riluzole’s Synaptic Protection Mechanism Through HSF1-BDNF Axis"],"thesis:degree_discipline":["Biomedical Sciences"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science (MS)"]},"updated_at":"2026-07-24T05:00:33Z"}