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. 2021 Apr 23;12:2421. doi: 10.1038/s41467-021-22624-z

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a Aβ40 (orange) and Aβ42 (blue) quantity in hAβ-KI homozygous mice was determined using the MSD V-PLEX Plus Aβ Peptide Panel 1 (6E10) Kit (n = 5 in 2 mo and 6 mo and n = 6 in 10 mo, 14 mo, 18 mo and 22 mo). The ELISA analysis shows that hAβ-KI mice produce high soluble Aβ levels, including Aβ40 (One-way ANOVA, F_5,28 = 10.01, Tukey’s post hoc test, *p < 0.05, **p < 0.01 and ***p < 0.001) and Aβ42 (One-way ANOVA, F_5,28 = 8.057, Tukey’s post hoc test, *p < 0.05, **p < 0.01 and ***p < 0.001) compared to old hAβ-KI mice (a1 and a2). Opposite effect is observed in insoluble Aβ levels in older hAβ-KI mice compared to younger hAβ-KI mice, including in Aβ40 (One-way ANOVA, F_5,28 = 7.21, Tukey’s post hoc test, *p < 0.05 and **p < 0.01) and Aβ42 (One-way ANOVA, F_5,28 = 6.543, Tukey’s post hoc test, *p < 0.05 and **p < 0.01) (a3-a4). b Aβ-PMCA shows accelerated in vitro aggregation using hAβ-KI (green) and 3xTg-AD (red) brain homogenate to seed monomeric Aβ compared to WT (blue) controls (n = 4/genotype). c Shorter time to reach 50% of total aggregation, measured by thioflavin-T emission levels (n = 4/genotype) (One-way ANOVA, F_2,11 = 9.083; Tukey’s post hoc test, *p < 0.05 and **p < 0.01). d Immunohistochemistry performed with Aβ40 and Aβ42 antibodies showed no sign of aggregates (plaques) for Aβ isoforms in hAβ-KI mice at 22-month of age (d4–d6). As a positive control, 3xTg-AD mice were used with significant Aβ40 and Aβ42 aggregates present at 22-month of age (d7–d9). WT mice showed no staining for both Aβ isoforms (d1–d3). 22-month-old hAβ-KI mice and 3xTg-AD mice were stained with thioflavin-S (Thio-S) (e) or Congo Red (f) stain. No fibrillar aggregated stained with Thio-S or Congo red is observed in hAβ-KI (e1 and f1). As a positive control, 3xTg-AD mice were used with fibrillary extracellular aggregates positive for Thio-S and Congo Red present in the hippocampus (e2 and f2). Data are presented as mean values ± SEM. Scale bar: 200 μm (e1, e2, f1 and f2), 100 μm (d1–d9) and 50 μm (e1b, e2b, f1b and f2b).