2026-06-30T01:23:00Zhttps://docta.ucm.es/rest/oai/request
oai:docta.ucm.es:20.500.14352/727122024-04-09T14:28:14Zcom_20.500.14352_14col_20.500.14352_15
Docta Complutense author Abascal, Maria Luisa author Sanjuan, Javier author Moyano-Cires Ivanoff, Paula Viviana author Sola Vendrell, Emma author Flores, Andrea author García Sánchez, José Manuel author García Lobo, Jimena author Frejo Moya, María Teresa author Pino Sans, Javier Del 2023-06-22T12:30:26Z 2023-06-22T12:30:26Z 2022-11-17 0893-228X 10.1021/acs.chemrestox.2c00278 https://hdl.handle.net/20.500.14352/72712 https://doi.org/10.1021/acs.chemrestox.2c00278 Acute and long-term paraquat (PQ) exposure produces hippocampal neurodegeneration and cognition decline. Although some mechanisms involved in these effects were found, the rest are unknown. PQ treatment, for 1 and 14 days, upregulated interferon-gamma signaling, which reduced insulin levels and downregulated the insulin pathway through phosphorylated-c-Jun N-terminal-kinase upregulation, increasing glucose levels and the production of Aβ1–42 and phosphorylated-tau, by beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) overexpression and phosphorylated-GSK3β (p-GSK3β; ser9) level reduction, respectively, which induced primary hippocampal neuronal loss. This novel information on the PQ mechanisms leading to hippocampal neurodegeneration could help reveal the PQ actions that lead to cognition dysfunction. eng Atribución 3.0 España Insulin Signaling Disruption and INF-γ Upregulation Induce Aβ1–42 and Hyperphosphorylated-Tau Proteins Synthesis and Cell Death after Paraquat Treatment of Primary Hippocampal Cells journal article URL https://docta.ucm.es/bitstreams/fa9e4171-8e16-4b3c-9179-6c13fcd40d69/download File MD5 51dec1b416228ae1efe25423cec03a08 1962791 application/pdf acs.chemrestox.2c00278.pdf URL https://docta.ucm.es/bitstreams/d8eb6353-012d-44be-92a6-83aa400b667f/download File MD5 2e3038ac155106647ad14255a750f62c 39157 text/plain acs.chemrestox.2c00278.pdf.txt