Amyloid pathology in APP/PSEN1 and APP/PSEN1/APOEnull mice.

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Amyloid pathology in APP/PSEN1 and APP/PSEN1/APOEnull mice. Amyloid pathology in APP/PSEN1 and APP/PSEN1/APOEnull mice. (A) Representative images of the global amount of amyloid in the cortex of APP/PSEN1 and APP/PSEN1/APOEnull mice at 10-mo old after anti-Aβ immunostaining (IH). As shown in the lower panels, the overall load of amyloid was comparable between genotypes, but the amount of dense-core plaques detected with Methoxy-XO4 was greatly diminished in the absence of APOE. (B) Scatter dot plot representing the stereological quantification of amyloid load in APP/PSEN1 and APP/PSEN1/APOEnull animals (including both adult and aged cohorts) after anti-Aβ immunostaining or Methoxy-XO4 labeling. (C) Scatter dot plots representing the stereological quantification of plaque density in APP/PSEN1 and APP/PSEN1/APOEnull animals. (D) The ratios of IH/Methoxy calculated per mouse showed that the amyloid deposits are mostly diffuse in APP/PSEN1/APOEnull mice as compared with APP/PSEN1. (E) The biochemical quantification of the concentrations of TBS-soluble Aβ40 and Aβ42 revealed lower levels of Aβ peptides in mice devoid of APOE as compared with APP/PSEN1 mice (both age groups pooled together). (F) A parallel result was observed when quantifying the levels of FA Aβ40 and Aβ42. (G) A similar difference was observed when the concentration of Aβ oligomers was measured from TBS brain extracts. Scale bar = 1,000 μm. n = 10 to 18 mice/group; unpaired t test; *P < 0.05, **P < 0.001, ***P < 0.0005. Eloise Hudry et al. LSA 2019;2:e201900325 © 2019 Hudry et al.