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. 2018 May 3;9:1784. doi: 10.1038/s41467-018-04120-z

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© The Author(s) 2018

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. 5 — Overexpression of C/EBPβ in young 3xTg mice accelerates the onset of AD-like pathogenesis and worsens cognitive dysfunctions. a Overexpression of C/EBPβ escalates delta-secretase and APP and Tau cleavage. Hippocampal tissues were analyzed by immunoblotting. C/EBPβ-induced active delta-secretase was antagonized by the co-expression of C189S mutant (n = 3 mice per group). b, c Overexpression of C/EBPβ but not C/EBPα increases delta-secretase mRNA and enzymatic activities. Data represent mean ± s.e.m. of three mice per group (*P < 0.05, **P < 0.01, one-way ANOVA). d Overexpression of C/EBPβ but not C/EBPα increases the expression of inflammatory cytokines. Data represent mean ± s.e.m. of three mice per group (*P < 0.05, one-way ANOVA). e C/EBPβ overexpression enhances the early formation of amyloid plaques in 3xTg mice. Thioflavin S staining for the senile plaques (top, scale bar, 50 μm). Analysis data (middle) represent mean ± s.e.m. of 12–18 sections from three mice per group and Aβ ELISA (lower) represent mean ± s.e.m. of three mice per group (*P < 0.05, **P < 0.01, one-way ANOVA). f Overexpression of C/EBPβ decreases dendritic spine density. Golgi staining was conducted on brain sections from apical dendritic layer of the CA1 region. Scale bar, 5 μm. Data (right) represent mean ± s.e.m. of 9–12 sections from three mice in each group. (*P < 0.05, one-way ANOVA). g Electrophysiology analysis. C/EBPβ overexpression worsened the LTP defects in 3xTg mice. The ratio of paired pulses (mean ± s.e.m.; n = 6 in each group; *P < 0.05 compared with 3xTg-Ct, ^#P < 0.05 compared with 3xTg-C/EBPβ+AEP C189S, one-way ANOVA) (left). LTP of fEPSPs (mean ± s.e.m.; n = 6 in each group; *P < 0.05 compared with 3xTg-Ct, ^#P < 0.05 compared with 3xTg-C/EBPβ+AEP C189S, one-way ANOVA) (right). Shown traces are representative fEPSPs of 10 samples recorded before (black) and after (red) TBS (theta-burst stimulation). 1, WT-Ct; 2, WT-C/EBPβ OE; 3, 3xTg-Ct; 4, 3xTg-C/EBPβ OE; 5, 3xTg-C/EBPβ+C189S AEP. h, i Morris water maze analysis. C/EBPβ overexpression exacerbated the learning and memory dysfunctions (mean ± s.e.m.; n = 7–8 mice per group; *P < 0.05, one-way ANOVA)