Fig. 10

Mechanism with which TgCtwh6 infection induces mouse cognitive behavior disorder at the cellular and molecular level in our experiments. First, in vivo, each C57BL/6 mouse was infected orally with TgCtwh6 cysts. On day 90 post-infection, the infected mice manifested cognitive behavioral abnormalities. The infected mouse hippocampal tissue assay showed that neurons were disorganized in the arrangement, decreased in the number and abnormally stained in nuclei. Moreover, apoptotic cells and Aβ protein increased in the infected mouse hippocampus (A). TgCtwh6 tachyzoites led to HT22 apoptosis following HT22 infection for 24 h; meanwhile, TgCtwh6 tachyzoites promoted BACE1, APP and Aβ production by activating NF-κB signaling pathway in HT22. Additionally, after BV2 cells had been infected by TgCtwh6 tachyzoites for 24 h, they could drive polarization to M1 through Notch signaling pathway with production of pro-inflammatory factors, which provoked co-cultured HT22 apoptosis and APP expression (B)