The quantitative relationship between the in-vivo signal of amyloid-β (Aβ) positron emission tomography (PET) imaging with [11C]6-OH-BTA-1 (PiB) in transgenic mouse models of Alzheimer's disease and the underlying histopathology is so far ill-defined. In this study we compared a single transgenic APP (Tg2576) and a double transgenic APP/PS1 mouse model (ARTE10). We performed PiB PET imaging followed by an automated quantification of Aβ plaque histopathology using three different stainings: Thioflavin S (TfS), immunofluorescence against full-length Aβ peptide, and against N3-pyroglutamate-Aβ peptide (N3pE-Aβ). PET images were analysed with a region-of-interest-based and a voxel-based approach. We found the highest correlation between TfS plaque load and PET results. Voxel-based analysis revealed a pattern of significant voxels which resembles the pattern of Aβ plaque distribution in the mouse brain. Our results suggest that the amount of high-dense TfS positive plaques but not the amount of diffuse TfS negative plaques is the determining factor for in-vivo PiB imaging. The presence of N3pE-Aβ did not relevantly influence the PET signal.
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