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. 2019 Jun 24;9:9116. doi: 10.1038/s41598-019-45547-8

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© The Author(s) 2019

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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Tau may regulate NMDA receptor trafficking through actin depolymerization. As discussed in the text, Tau phosphorylated could facilitate F-actin depolymerization in the spine in a direct or indirect way, and as consequence of that, synapytic NMDA receptors could move to extrasynaptic regions. This effect may not take place in Tau^−/− mice.