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Figure 2 | Acta Neuropathologica Communications

Figure 2

From: Mild chronic cerebral hypoperfusion induces neurovascular dysfunction, triggering peripheral beta-amyloid brain entry and aggregation

Figure 2

Hypoperfusion triggers vascular deposition of peripherally applied human Aβ 1-42 peptides. 1% Thioflavin S (A), combined with immunofluorescence (C) and double immunofluorescence (D) analysis examining the deposition of Aβ aggregates, and their sub-cellular localization in brain capillaries 24 hours after Aβ1-42 administration in mice that were hypoperfused for 24 hours. (A, B) Thioflavin S positive Aβ deposits are observed in ipsilateral brain capillaries of the cortex and hippocampus, and are almost absent in contralateral brain capillaries of the same animals, and in the brain capillaries of saline treated animals. (C) Thioflavin S positive Aβ deposits are localized in the perivascular space of brain capillaries within GFAP positive astrocytic endfeet. (D) Endothelial marker CD31, and Anti human 6E10 Aβ double staining confirm the vascular localization of Aβ deposits in ipsilateral brain capillaries. Data are means ± SEM (n = 5 animals per group, 5 sections per animal’s brain). Arrowheads show vascular Thioflavin S/6E10 positive aggregates.1 VO 24 H, one vessel occlusion for 24 hours. ****P < 0.0001 compared with contralateral hemisphere (two-tailed unpaired t-test's).

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