Fig. 5
From: Aβ43 aggregates exhibit enhanced prion-like seeding activity in mice
Induced Aβ42 deposition in AppNL−F mice inoculated with recombinant Aβ43 aggregates. a Schematic of the locations of induced Aβ pathology in the brains of AppNL−F mice. b Semi-quantitative scoring of Aβ42 pathology (12F4 immunohistochemistry) in mice at 6 months post-inoculation with recombinant Aβ aggregates (n = 6, 8, 10, or 8 for Aβ38, Aβ40, Aβ42, and Aβ43, respectively) or purified brain-derived Aβ aggregates from either TgCRND8 (n = 9) or AppNL−F (n = 9) mice. Mice inoculated with either dH2O (n = 5) or material derived from a non-Tg mouse brain (n = 6) were used as negative controls. Compared to mice injected with dH2O, there was a significant increase in Aβ42 pathology in the cerebellum of mice injected with Aβ43 aggregates (P = 0.00029), in the occipital cortex of mice inoculated with AppNL−F Aβ aggregates (P = 0.0039), in the olfactory bulb of mice inoculated with AppNL−F Aβ aggregates (P = 0.022), and in the subcallosal region of mice inoculated with AppNL−F (P = 0.0022) or TgCRND8 (P = 0.022) Aβ aggregates, as determined by a Kruskal–Wallis test followed by Dunn’s multiple comparisons test. c Representative images of Aβ42 pathology (12F4 immunohistochemistry) in the occipital cortex, subcallosal region, and cerebellum of AppNL−F mice at 6 months post-inoculation with the indicated Aβ preparations. Red arrows indicate minor amounts of Aβ deposition in the subcallosal region of Aβ43-inoculated mice and the cerebellum of Aβ42-inoculated mice. Scale bars = 50 µm (applies to all images)