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. 2021 Sep 30;9:162. doi: 10.1186/s40478-021-01259-7

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — Increased pathological PKA-mediated tau phosphorylation in Tau mice lacking PS. Left: Representative immunohistochemical images of phosphorylated tau (PG5: pSer409) in 6 month-old non- and tau transgenic mice. Inset: magnified images showing somatic PG5 staining in PS cKO;Tau brains. Scale bar: 100 μm. Right: Quantitative analysis of number of PG5-positive cells/section in the indicated brain region in littermate control (WT), Tau, PS1 cKO;Tau and PS cKO;Tau mice. Values represent mean PG5-positive cells ± s.e.m. (3 slices per mouse, 4–5 mice/group). Statistical analysis was determined by two-way ANOVA followed by Tukey’s post hoc tests. *P < 0.05, **P < 0.01, ***P < 0.001. Abbreviations: Amygdala: basolateral amygdala; CA1/CA3 hippocampus; DG, dentate gyrus; EC, entorhinal cortex; RSC, retrosplenial cortex