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.
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