Figure 5

Genetic ablation of β-arrestin1 ameliorates memory deficits in AD mice. (A, B) The β-arrestin1 deficiency rescues recognition memory deficit in APP/PS1 mice (n = 7-9 for each group). Preference score (A) was the percentage of time that mice spent on exploring one of the two identical familiar objects in training session; recognition index (B) was the time that mice spent on exploring a novel versus a familiar object during a 10 min test session. (C) Learning curves during hidden platform training in MWM. The latency of each mouse to reach the hidden platform was recorded. (D) Time that took mice to search in the target quadrant in probe trial on day 11 was recorded. (E) Representative tracks of each genotype of mice in probe trial on day 11 were shown. “T” represents the target quadrant where the platform used to be. (F) The swimming distance (upper panel) and velocity (lower panel) remain unchanged upon APP/PS1 transgene or β-arrestin1 knockout. ^*P < 0.05, ^***P < 0.001.