RT Journal Article
T1 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
A1 Abascal, Maria Luisa
A1 Sanjuan, Javier
A1 Moyano-Cires Ivanoff, Paula Viviana
A1 Sola Vendrell, Emma
A1 Flores, Andrea
A1 García Sánchez, José Manuel
A1 García Lobo, Jimena
A1 Frejo Moya, María Teresa
A1 Pino Sans, Javier Del
AB 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.
PB ACS Publications
SN 0893-228X
YR 2022
FD 2022-11-17
LK https://hdl.handle.net/20.500.14352/72712
UL https://hdl.handle.net/20.500.14352/72712
LA eng
NO CRUE-CSIC (Acuerdos Transformativos 2022)
NO Universidad Complutense de Madrid/Banco de Santander
DS Docta Complutense
RD 5 abr 2025