This study investigated the molecular mechanisms underlying chemotherapy-induced cognitive impairment (CICI) following doxorubicin and cyclophosphamide treatment in a rat model, revealing three significant alterations in hippocampal tissue: selective downregulation of heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) (21% decrease, p=0.0298), compromised astrocytic network integrity evidenced by reduced GFAP-positive area in cornu ammonis 3 (CA3) (24%, pB=0.026) and dentate gyrus (DG) (19%, pB=0.027) regions, and elevated cellular senescence marker p19Arf specifically in DG (69%, pB=0.033) and CA3 (27%, pB=0.024). The inverse relationship between hnRNPA1 reduction and p19Arf elevation suggests a potential mechanistic link between RNA dysregulation and senescence induction, with pronounced vulnerability in regions critical for adult neurogenesis and memory processing, thereby providing molecular targets for developing neuroprotective strategies to mitigate cognitive impairment in cancer patients undergoing chemotherapy.
","abstract_html":"<p>This study investigated the molecular mechanisms underlying chemotherapy-induced cognitive impairment (CICI) following doxorubicin and cyclophosphamide treatment in a rat model, revealing three significant alterations in hippocampal tissue: selective downregulation of heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) (21% decrease, p=0.0298), compromised astrocytic network integrity evidenced by reduced GFAP-positive area in cornu ammonis 3 (CA3) (24%, pB=0.026) and dentate gyrus (DG) (19%, pB=0.027) regions, and elevated cellular senescence marker p19Arf specifically in DG (69%, pB=0.033) and CA3 (27%, pB=0.024). The inverse relationship between hnRNPA1 reduction and p19Arf elevation suggests a potential mechanistic link between RNA dysregulation and senescence induction, with pronounced vulnerability in regions critical for adult neurogenesis and memory processing, thereby providing molecular targets for developing neuroprotective strategies to mitigate cognitive impairment in cancer patients undergoing chemotherapy.<strong></strong></p>","abstract_has_math":false,"creators":["Chen, Lijie"],"institution":null,"degree_name":"Master of Science (M.S.)","degree_level":"Thesis","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":["Karen Hubbard","Jonathan levitt","Mark Emerson"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2025,"date_issued":"2025-01-01T08:00:00Z","date_published":"2025-01-01T08:00:00Z","updated_at":"2026-07-24T01:58:07Z","subjects":["HnrnpA1","Hippocampus","Doxorubicin","cyclophosphamide","Chemotherapy induced cognitive impairment","Neurons","Biology","Cognitive Neuroscience","Molecular and Cellular Neuroscience","Neuroscience and Neurobiology"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://academicworks.cuny.edu/cc_etds_theses/1194","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Karen Hubbard","Jonathan levitt","Mark Emerson"]},{"key":"dc:creator","label":"Author","values":["Chen, Lijie"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2025-05-06T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science (M.S.)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["HnrnpA1","Hippocampus","Doxorubicin","cyclophosphamide","Chemotherapy induced cognitive impairment","Neurons","Biology","Cognitive Neuroscience","Molecular and Cellular Neuroscience","Neuroscience and Neurobiology"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://academicworks.cuny.edu/cc_etds_theses/1194"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["This study investigated the molecular mechanisms underlying chemotherapy-induced cognitive impairment (CICI) following doxorubicin and cyclophosphamide treatment in a rat model, revealing three significant alterations in hippocampal tissue: selective downregulation of heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) (21% decrease, p=0.0298), compromised astrocytic network integrity evidenced by reduced GFAP-positive area in cornu ammonis 3 (CA3) (24%, pB=0.026) and dentate gyrus (DG) (19%, pB=0.027) regions, and elevated cellular senescence marker p19Arf specifically in DG (69%, pB=0.033) and CA3 (27%, pB=0.024). The inverse relationship between hnRNPA1 reduction and p19Arf elevation suggests a potential mechanistic link between RNA dysregulation and senescence induction, with pronounced vulnerability in regions critical for adult neurogenesis and memory processing, thereby providing molecular targets for developing neuroprotective strategies to mitigate cognitive impairment in cancer patients undergoing chemotherapy.
"]},{"key":"dc:title","label":"Title","values":["Investigation of RNA-Binding Protein Expression Changes in the Hippocampus Following Doxorubicin and Cyclophosphamide Treatment"]}]}],"canonical_facts":{"dc:contributor":["Karen Hubbard","Jonathan levitt","Mark Emerson"],"dc:creator":["Chen, Lijie"],"dc:date.available":["2025-05-06T07:00:00Z"],"dc:description.abstract":["This study investigated the molecular mechanisms underlying chemotherapy-induced cognitive impairment (CICI) following doxorubicin and cyclophosphamide treatment in a rat model, revealing three significant alterations in hippocampal tissue: selective downregulation of heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1) (21% decrease, p=0.0298), compromised astrocytic network integrity evidenced by reduced GFAP-positive area in cornu ammonis 3 (CA3) (24%, pB=0.026) and dentate gyrus (DG) (19%, pB=0.027) regions, and elevated cellular senescence marker p19Arf specifically in DG (69%, pB=0.033) and CA3 (27%, pB=0.024). The inverse relationship between hnRNPA1 reduction and p19Arf elevation suggests a potential mechanistic link between RNA dysregulation and senescence induction, with pronounced vulnerability in regions critical for adult neurogenesis and memory processing, thereby providing molecular targets for developing neuroprotective strategies to mitigate cognitive impairment in cancer patients undergoing chemotherapy.
"],"dc:identifier":["https://academicworks.cuny.edu/cc_etds_theses/1194"],"dc:subject":["HnrnpA1","Hippocampus","Doxorubicin","cyclophosphamide","Chemotherapy induced cognitive impairment","Neurons","Biology","Cognitive Neuroscience","Molecular and Cellular Neuroscience","Neuroscience and Neurobiology"],"dc:title":["Investigation of RNA-Binding Protein Expression Changes in the Hippocampus Following Doxorubicin and Cyclophosphamide Treatment"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science (M.S.)"]},"updated_at":"2026-07-24T01:58:07Z"}