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. 2018 Nov 20;8:17081. doi: 10.1038/s41598-018-35114-y

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© The Author(s) 2018

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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p66Shc activation enhances Aβ toxicity. (A) Treatment of B12 cells with both Aβ_1–42 (20 µM) and DOPPA (100 nM) was significantly more toxic than Aβ treatment alone. (B) Silencing of p66Shc expression in B12 cells led to reduced Aβ-induced toxicity compared to B12 cells transfected with control siRNA and treated with Aβ. (C) HT22 cells ectopically expressing p66Shc and treated with DOPPA (100 nM) exhibited significantly decreased viability following Aβ treatment compared to pcDNA control cells treated with both agents. (D) DOPPA induced activation of p66Shc exacerbated Aβ toxicity in mouse primary cortical neurons. Data presented are the mean ± SEM of 3 independent experiments (*P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001).