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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. 2.

Fig. 2

Effects of PERK haploinsufficiency on memory deficits and cholinergic neurodegeneration in 5XFAD mice. (A, B) Mice were trained with two CS-US pairings for contextual fear conditioning (wild-type, n = 22; PERK+/−, n = 24; 5XFAD, n = 28; PERK+/−·5XFAD, n = 27). Freezing behavior was assessed during training session (B) as well as 24-h memory retention test (A). 5XFAD mice showed significantly lower levels of contextual freezing than wild-type mice when tested 24 h after training. Note that PERK+/−·5XFAD mice were rescued almost completely back to wild-type control levels of contextual memory. (C) Brain sections were immunostained for the cholinergic marker ChAT. Shown are representative photomicrographs of ChAT-immunoreactive neurons in the medial septum of mice. Scale bar = 200 μm. (D) The number of ChAT-positive neurons in the medial septum and the vertical limb of the diagonal band (Ch1/2), which provide the cholinergic innervation to the hippocampus, was counted for quantification (wild-type, n = 4; 5XFAD, n = 4; PERK+/−·5XFAD, n = 5). Note that PERK haploinsufficiency almost completely prevented cholinergic neurodegeneration 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).