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. 2021 Jan 20;13:30. doi: 10.1186/s13195-020-00745-9

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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. 5 — Effects of generalized immunosuppression on soluble and epigenetic markers of neurodegeneration. a Representative western blot illustrating total tau, phosphorylated tau, and β-actin protein levels in TBS homogenates extracted from the cortex of 6-month-old mice. b Densitometric analysis of western blots revealed that 6-month-old 3xTg-AD females had elevated levels of TBS-soluble total tau (normalized to β-actin) in comparison to WT controls, but this genotype-related difference was not noted in males (Genotype × Sex: F_{1, 81} = 18.77, p < .001) and was not altered by CY immunosuppression. c 3xTg-AD females also exhibited an increase in phospho-tau (Thr181) in comparison to all other groups (Genotype × Sex: F_{1, 81} = 16.354, p < .001), but CY had no appreciable effect on the phosphorylation status of tau. d Soluble human Aβ₄₂ was greater in 3xTg-AD males than females (Genotype × Sex: F_{1, 68} = 8.921, p = .004, η2p = .116). No significant third order interaction was detected, but between-group comparisons with t tests revealed that CY-treated 3xTg-AD males had lower Aβ₄₂ load than Veh-treated controls (p < .01). e BDNF mRNA levels were downregulated in 3xTg-AD mice of both sexes compared to controls. CY did not affect BDNF mRNA levels (normalized to β-actin) in 3xTg-AD mice. f 3xTg-AD mice treated with vehicle only had significantly higher H2afy mRNA expression compared to controls (p < .0001). CY treatment reversed the upregulated H2afy expression observed in vehicle-treated 3xTg-AD mice compared to WT mice (p = .046). No significant third order interaction was detected, but between-group comparisons with t tests revealed H2afy downregulation in CY-treated 3xTg-AD females. WT Veh males (n = 11), WT CY males (n = 11), 3xTg-AD Veh males (n = 9), 3xTg-AD CY males (n = 9), WT Veh females (n = 13), WT CY females (n = 14), 3xTg-AD Veh females (n = 10), 3xTg-AD CY females (n = 11). Overall group comparisons were carried out using three-way ANOVA (Genotype × Treatment × Sex), followed by post hoc t tests. Error bars = SEM, *p ≤ .05, **p < .01, ***p < .001. Abbreviations: Aβ, amyloid-beta; BDNF, brain-derived neurotrophic factor; mRNA, messenger RNA; pTau, phosphorylated tau; tTau, total tau; TBS, tris-buffered saline