CD86 and infection: Fig 5C listed the representative activation makers regarding neuroinflammation. The infection led to the upregulation of both the activated markers (CD86, IL1β, and IL6; H2-D1, Ggta1, Fbln5, and Psmb8) associated with M1 microglia and A1 astrocytes [24, 57]. Furthermore, KEGG analysis showed that the top 2 enriched pathways were “Cytokine-cytokine receptor interaction” and “NF-kappa B signaling pathway” (Fig 5D). These results support that T. gondii infection triggers extensive neuroinflammation, thereby damaging the equilibrium in the prefrontal cortex of mice.