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. 2019 Dec 5;9:18393. doi: 10.1038/s41598-019-54846-z

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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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Efficacy of YU102 in Tg2576 mice is independent of Aβ deposition and tau aggregation. (a) ELISA-based quantification of Aβ_1–42 in hippocampal tissues isolated from Tg2576 mice. The difference in the levels of Aβ_1–42 between vehicle control and YU102-treated mice was not statistically significant (p-value > 0.1, n = 3). Statistical analysis of ELISA results was performed via Student’s t-test. (b) Thioflavin T staining of Aβ fibrils in hippocampal tissue sections from Tg2576 mice. (c) YU102 has no effect on tau aggregation. Thapsigargin induces tau aggregation in HEK 293 tau-BiFC cells, activating a tau BiFC fluorescence signal that can be detected. (d) YU102 displays no neuroprotective effects during the experimental period. Hippocampal tissues isolated from the brains of Tg2576 mice were stained with Cresyl violet, a marker for Nissl substance in neurons.