ApoE4-Driven Accumulation of Intraneuronal Oligomerized Aβ42 following Activation of the Amyloid Cascade In Vivo Is Mediated by a Gain of Function
Figure 4
The effects of apoE3, apoE4, and apoE deficiency on the mitochondria of hippocampal CA1 neurons following inhibition of neprilysin. ApoE3, apoE4, and apoE-deficient male mice were injected i.c.v. with the neprilysin inhibitor thiorphan or sham-treated for 10 days, after which their brains were excised and subjected to COX-1 immunofluoresence as described in “Materials and Methods.” (a) Representative coronal sections of sham- and thiorphan-treated apoE-deficient mice (upper row) and thiorphan-treated apoE3 and apoE4 mice (lower row) immunostained with anti-COX-1 are shown on the left ( μm). Quantification of the density of staining (; mice/group in the sham- and thiorphan-treated groups) in the CA1 neurons of the indicated mice is shown on the right (empty and filled bars correspond, resp., to sham- and thiorphan-treated mice). for the effects of treatment on the three mouse groups by Two-way ANOVA. (b) Representative confocal images of the co-localization of Aβ42 and COX-1 in the CA1 area of apoE-deficient mice treated with thiorphan for 10 days.
