Fig. 3
From: Restoring synaptic plasticity and memory in mouse models of Alzheimer’s disease by PKR inhibition
PKRi treatment does not decrease Aβ1–42 in the hippocampus of 5XFAD mice. a Representative immunoblots of protein extracts from the hippocampi 1 h after PKRi injection (0.335 mg/kg) in WT and 5XFAD mice. b, c Quantification of the of Aβ1–42 oligomers such as dimers and tetramers showing that PKRi treatment did not affect Aβ1–42 oligomers in 5XFAD mice (dimer levels normalized by that of 5XFAD; vehicle, 0; vehicle + PKRi, 0; Aβ1–42, 1.00 ± 0.15; Aβ1–42 + PKRi, 1.18 ± 0.06; unpaired t-test, 5XFAD vs 5XFAD + PKRi, p = 0.2674; tetramer levels normalized by that of 5XFAD; vehicle, 0; vehicle + PKRi, 0; Aβ1–42, 1.00 ± 0.13; Aβ1–42 + PKRi, 1.28 ± 0.23; unpaired t-test, 5XFAD vs 5XFAD + PKRi, p = 0.3243; 6 hippocampi from 3 mice per group). Bars represent as mean ± SEM