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. Author manuscript; available in PMC: 2015 Oct 1.
Published in final edited form as: Neurobiol Aging. 2014 May 2;35(10):2272–2281. doi: 10.1016/j.neurobiolaging.2014.04.031

Fig. 3.

Fig. 3

Effects of PERK haploinsufficiency on β-amyloidogenic processing of APP and Aβ accumulation in 5XFAD mice. (A) Representative immunoblots of protein extracts from hippocampal homogenates of mice. (B, C) Immunoreactive bands were quantified and expressed as the percentage of 5XFAD (B) or wild-type control (C) mice (wild-type, n = 6; 5XFAD, n = 8; PERK+/−·5XFAD, n = 8). Note that PERK haploinsufficiency significantly reduced levels of BACE1, full-length APP and C99, while it restored decreased neprilysin expression in 5XFAD mice. (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 (5XFAD, n = 9; PERK+/−·5XFAD, n = 12). (E) Brain sections were immunostained with the 6E10 anti-Aβ antibody. Shown are representative photomicrographs of the hippocampal and cortical regions. Scale bar = 500 μm. (F) Percentage area occupied by Aβ deposits in the hippocampus and cerebral cortex was measured for quantification (5XFAD, n = 7; PERK+/−·5XFAD, n = 5). PERK haploinsufficiency significantly reduced Aβ40 and Aβ42 concentrations as well as plaque burden in 5XFAD mice. All data are presented as mean ± SEM and were analyzed by one-way ANOVA followed by post-hoc Fisher’s PLSD test (* p < 0.05 vs. wild-type, # p < 0.05 vs. 5XFAD).