Deletion of the eIF2α Kinase GCN2 Fails to Rescue the Memory Decline Associated with Alzheimer’s Disease (original) (raw)
Figure 2
Effects of GCN2 deletion on Aβ load and plaque-associated elevation of BACE1 expression in 5XFAD mice.
(A) Brain sections were immunostained with the 6E10 anti-Aβ antibody. Shown are representative photomicrographs of the hippocampal region. Scale bar = 500 µm. (B) Percentage area occupied by Aβ deposits in the hippocampus was measured for quantification (n = 6–8). GCN2−/− deletion exacerbates plaque burden in 5XFAD mice (#p<0.05 vs. 5XFAD). Data are presented as mean ± SEM. (C) Double immunofluorescence labeling with 6E10 anti-Aβ (green) and anti-BACE1 (red) antibodies (n = 3–4). Note the high degree of colocalization of Aβ and BACE1 immunoreactivities in the hippocampus of 5XFAD and GCN2−/−·5XFAD mice. Scale bar = 50 µm.