Fig. 2

β-amyloid pathology is mitigated in female APP/PS1 mice carrying the PLCγ2-P522R variant. A X-34-positive β-amyloid plaque count (*p = 0.005) and coverage (**p = 0.006, total plaque area, % of whole analyzed area) were lower in the entorhinal cortex of APP/PS1xPLCγ2-P522R (A+/P^ki/ki) mice than in that of APP/PS1 (A+/P^wt/wt) mice. The size (µm²) of the individual plaques did not differ between the genotypes. A+/P^wt/wt n = 4 and A+/P^ki/ki n = 6. B Insoluble but not soluble Aβ40 and −42 levels are slightly but not significantly lower in the temporo-occipital cortex of A+/P^ki/ki mice than in that of A+/P^wt/wt mice. Aβ40 and Aβ42 levels were normalized to the total protein concentration in the same sample. A+/P^wt/wt n = 4 and A+/P^ki/ki = 4. C Representative Western blots and corresponding quantification showing no differences in the levels of full-length APP (APPtot, normalized to GAPDH), APP C-terminal fragments (C99 and C83, normalized to APPtot), or soluble APPα and APPβ (sAPPα, sAPPβ, normalized to APPtot) species in the temporo‒occipital cortex of A+/P^ki/ki and A+/P^wt/wt mice. A+/P^wt/wt n = 4 and A+/P^ki/ki n = 4. The scale bars in the representative immunofluorescence images are 657 µm for the whole area and 164 µm for the zoomed view. Unpaired samples t test. All the data are presented as the means ± SEMs. Each data point represents an individual mouse