Fig. 6
From: Restoring synaptic plasticity and memory in mouse models of Alzheimer’s disease by PKR inhibition
PKRi treatment has a trend to reverse Aβ1–42-mediated changes in PKR signaling. a Representative immunoblots of protein extracts from hippocampi 30 min after PKRi injection (0.335 mg/kg) in Aβ1–42-treated mice. b PKRi treatment showed a trend to decrease eIF2α phosphorylation in Aβ1–42-treated mice, but the effect was not statistically significant (normalized p-PKR, vehicle, 1.00 ± 0.05, 14, 14 hippocampi from 11 mice; Aβ1–42, 1.22 ± 0.09, 15 hippocampi from 13 mice; Aβ1–42 + PKRi, 1.01 ± 0.06, 14 hippocampi from 11 mice; unpaired t-test, vehicle vs Aβ1–42, p = 0.055; Aβ1–42 vs Aβ1–42 + PKRi, p = 0.089). c PKRi treatment showed a trend to decrease eIF2α phosphorylation in Aβ1–42-treated mice, but the effect was not statistically significant (normalized p-eIF2α, vehicle, 1.00 ± 0.04, 17 hippocampi from 11 mice; Aβ1–42, 1.28 ± 0.11, 19 hippocampi from 13 mice; Aβ1–42 + PKRi, 1.14 ± 0.10, 18 hippocampi from 12 mice; unpaired t-test, vehicle vs Aβ1–42, *p < 0.05; Aβ1–42 vs Aβ1–42 + PKRi, p = 0.354). (D) CREB phosphorylation was slightly reduced by Aβ1–42 and was rescued by PKRi treatment although it was not statistically significant (normalized p-CREB, vehicle, 1.00 ± 0.07, 15 hippocampi from 9 mice; Aβ1–42, 0.93 ± 0.05, 15 hippocampi from 9 mice; Aβ1–42 + PKRi, 1.01 ± 0.07, 16 hippocampi from 10 mice; unpaired t-test, vehicle vs Aβ1–42, p = 0.426; Aβ1–42 vs Aβ1–42 + PKRi, p = 0.390). Bars represent as mean ± SEM