Expression of human tau increases amyloid plaque burden.
(a) Low-magnification view of horizontal brain sections from APP/PS1 and rTgTauEC x APP/PS1 mice at 10 months of age (Top) and APP/PS1, rTgTauEC x APP/PS1 and control mice at 16 months of age (Bottom), immunostained with AW7 antibody to visualize amyloid plaques. Regions of interest are outlined in white on control (neuropsin promotor only) image (scale bar = 1 mm). (b) Top: Quantification of amyloid plaque area revealed significantly larger plaques in rTgTauEC x APP/PS1 mice compared with APP/PS1 mice the EC in 10- and 16 months of age, and in the somatosensory cortex at 16 months of age. Bottom: The number of amyloid plaques was also increased in 16-month-old rTgTauEC x APP/PS1 mice in both the EC and somatosensory cortices (10 months: APP/PS1, N = 7; rTgTauEC x APP/PS1, N = 7. 16 months: APP/PS1, N = 4; rTgTauEC x APP/PS1, N = 11). (c) Expression of human APP transgene was assessed by qPCR. No differences in APP mRNA were observed in 16-month-old APP/PS1 vs. rTgTauEC x APP/PS1 mice (APP/PS1, N = 3; rTgTauEC x APP/PS1, N = 5). Values represent mean ± s.e.m; *P < 0.05, **P < 0.01, ***P < 0.001.