Fig. 4
From: Restoring synaptic plasticity and memory in mouse models of Alzheimer’s disease by PKR inhibition
PKRi treatment rescues memory deficit in novel object recognition (NOR) in Aβ1–42–injected mice. Injection of Aβ1–42 oligomers (3 μg/mouse) induced NOR memory deficit, which was rescued by PKRi treatment. PKRi (0.335 mg/kg) was intraperitoneally injected 20 min before NOR training (Preference index for the novel object: Vehicle, 61.33 ± 2.85%; PKRi, 60.92 ± 0.83%; Aβ, 49.09 ± 3.21%; Aβ1–42 and PKRi, 62.7 ± 2.79%; Two-way ANOVA, interaction between Aβ1–42 and PKRi, *p < 0.05; Bonferroni post-tests, *p < 0.05, **p < 0.01, n = 6 mice for each group). Bars represent as mean ± SEM