Cdc42GAP deficiency induced AD phenotypes in 11-month-old mice. (A–D) Immunofluorescence images (left) and quantification of the average optical density analyses (right) showed that the levels of phosphorylated Tau (p-T231) (A and B) and Tau (AT8) (C and D) in GAP, AD and GAP/AD mice were greater than those in wild-type (WT) mice in the hippocampus and cortex, and Cdc42GAP deficiency worsened tau phosphorylation in AD mice (n = 3 mice/group). (E–H) Immunofluorescence images (left) and quantification of the average optical density analyses (right) showed that Aβ_1–42 (E and F) and Aβ_1–40 (G and H) in GAP, AD and GAP/AD mice were significantly increased compared with those in wild-type mice and that Cdc42GAP deficiency worsened Aβ aggregation (n = 3 mice/group). (I–L) Representative western blots (I and J) and statistical analyses (right) revealed that the levels of Aβ_1–42 and Aβ_1–40 in the hippocampus (K) and cortex (L) from GAP and AD mice were elevated compared with those in wild-type mice (n = 3 mice/group). (M–P) ELISA analyses indicated that the levels of soluble (M) and insoluble (N) Aβ_1–42, and soluble (O) and insoluble (P) Aβ_1–40, were significantly increased in the hippocampus and cortex of GAP and AD mice compared with wild-type mice (n = 3 mice/group). One-way ANOVA was used across groups, and the least significant difference test was used for post hoc comparison. Error bars depict SEM. *P < 0.05, **P < 0.01, ***P < 0.001.