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Fig. 5 | Acta Neuropathologica Communications

Fig. 5

From: Exogenous Aβ seeds induce Aβ depositions in the blood vessels rather than the brain parenchyma, independently of Aβ strain-specific information

Fig. 5

Representative immunohistochemical images of R1.40 mice injected with autopsied human brain extracts. Representative images of the R1.40 mice injected with human brain extracts from the patients with Alzheimer’s disease (AD) (AD), cerebral amyloid angiopathy (CAA) (EH), AD + CAA (IL), and less amyloid β peptide (Aβ) pathology (MP), and PBS (QT). Antibodies against Aβ17–24 (4G8, 1:5,000) (A, E, I, M,, and Q), Aβ35–40 (1A10, 1:1,000) (B, F, J, N, and R), and Aβ1–42 (1:100) (C, G, K, O, and S) were used as primary antibodies for immunohistochemistry, and Congo red staining was also performed (D, H, L, P, and I). Diffuse Aβ plaques, not cored plaques, and CAA were observed in all groups of mice injected with human brain extracts (A, B, C, E, F, G, I, J, K, M, N, and O). The small inserts show diffuse Aβ plaques at high magnification (A, E, I, and M). Vessels with CAA were stained with Congo red, but few Congo red-positive lesions were observed in the brain parenchyma (D, H, L, and P). The small inserts show Congo red-positive vessels with high magnification (D, H, L, and P). In the group of the PBS-injected mice, neither Aβ plaques nor CAA were observed (QT). The scale bar represents 100 µm, and 25 µm for small inserts

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