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. 2020 Dec 14;141(2):217–233. doi: 10.1007/s00401-020-02249-0

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© The Author(s) 2020

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/.

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Fig. 4 — Tau kinase profile impact on AoO in PSEN1 E280A FAD. a Densitometric analysis in temporal cortex (TC) of basal and active forms of Tau kinases in controls (Control, n = 5), SAD (n = 10), E-AOFAD (n = 15), and LOFAD (n = 8). AKT/GSK3β pathway activation was significantly higher and MEK/ERK activation was lower in LOFAD when compared with E-AOFAD cases. Furthermore, JNK, Fyn, and mPPA2 steady-state levels were significantly different between LOFAD and E-AOFAD, while Fyn and mPPA2 levels were also significantly different between LOFAD and SAD cases (* = p ≤ 0.05, ** = p ≤ 0.01). b Logarithmic heatmap representation for significantly active or inactive kinases identified by microarray-based kinome profiling for Tyrosine (upper panel) and Serine/Threonine (lower panel) kinases in TC from Control (n = 3), SAD (n = 5), E-AOFAD (n = 10), and LOFAD (n = 5). LOFAD cases showed lower active Tyrosine kinases profile when compared with other groups. (FGFR4, RET, FGFR1, MERTK, EGFR, KIT, RYK, and other functionally related kinases; Supplementary Fig. 13A-B, online resource) and Serine/Threonine kinases (PDK1, MELK, MEK1, MEK2, MEK7, PKACb, PKCa, PKCb, PKCd, PKCe, PKCg, PKCt, HIPK2, HIPK3, HIPK4, AMPKa1, ANPa, and ZC2; Supplementary Fig. 14, online resource)