Figure 7.
Proposed pathway of NLRC3 mediation which contributes to AD. Aβ and APP/PS1 downregulated the expression of NLRC3 and consequently increased the PI3K expression and activation. PI3K-related functional proteins contributed to Aβ and APP/PS1-induced plaque deposition, glial cell activation, and neuron loss in AD. The NLRC3 overexpression inhibited the activation of PI3K; on the contrary, this effect of NLRC3 could be partially reversed by 740Y-P (PI3K agonist).