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. 2016 Jul 11;11:50. doi: 10.1186/s13024-016-0119-y

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 8 — Mechanism of the disease-modifying effect of P021 in AD. The CNTF small-molecule peptide mimetic compound, P021, increases BDNF expression which via the TrkB-PI3K-AKT pathway leads to inhibitory phosphorylation of GSK3β at Ser9 [99]. GSK3β is major tau kinase and contributes to abnormal hyperphosphorylation of tau at several major sites, and also plays a role in the amyloidogenic processing of APP. P021, via decreasing the GSK3β activity, causes decrease in tau and Aβ pathologies