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. 2013 Oct 11;8(10):e77335. doi: 10.1371/journal.pone.0077335

Figure 1. Effects of GCN2 deletion on memory deficits and β-amyloidogenic processing of APP in 5XFAD mice.

Figure 1

(A) GCN2−/− and GCN2+/− deficiencies had no effects on memory impairments in 5XFAD mice (*p<0.05 vs. wild-type), as tested by the contextual fear conditioning (n = 11–19). (B) Representative immunoblots of protein extracts from hippocampal homogenates of mice. (C) Immunoreactive bands were quantified and expressed as the percentage of 5XFAD control mice (n = 5–8). Note that GCN2 mutations further increase BACE1 and C99 levels without affecting APP overexpression in 5XFAD mice (*p<0.05 vs. wild-type, # p<0.05 vs. 5XFAD). (D) Levels of total Aβ40 and Aβ42 were quantified by sandwich ELISAs of guanidine extracts of hippocampal samples and expressed as the percentage of 5XFAD controls (n = 5–10). GCN2 mutations also significantly elevate Aβ40 and Aβ42 concentrations in 5XFAD mice (# p<0.05 vs. 5XFAD). All data are presented as mean ± SEM.