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Figure 5 | BMC Neuroscience

Figure 5

From: Detailed immunohistochemical characterization of temporal and spatial progression of Alzheimer's disease-related pathologies in male triple-transgenic mice

Figure 5

Amygdala-resident human APPswe transgene expression is slightly delayed, while Aβ peptide deposition evolves on a similar timescale as compared to the 3xTg-AD hippocampus. Coronal mouse brain sections (30 μm) were prepared from 3xTg-AD mice sacrificed at 2 (A, I, Q), 3 (B, J, R), 6 (C, K, S), 9 (D, L, T), 12 (E, M, U), 15 (F, N, V), 18 (G, O, W), and 26 months of age (H, P, X) and were processed for immunohistochemistry to detect the human Swedish mutant amyloid precursor protein (hAPPswe) transgene product using the Y188 monoclonal antibody (A–H), human amyloid precursor protein (hAPP) and Aβ peptides using the 6E10 monoclonal antibody (I-P), and extracellular Aβ1–42 deposition using the 12F4 monoclonal antibody (Q-X). Amygdala was examined for patterns of immunopositivity and photomicrographs were obtained at 10×. The insets in panels H, P, and X represent 40× digitally magnified images of designated photomicrographs for better visualization of immunopositive cell/pathology. Scale bar in D represents 200 μm.

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