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. 2019 Jan 24;9:544. doi: 10.1038/s41598-018-35811-8

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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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aSyn-mediated impairment in lysosomal activity and autophagosome turnover. (a,b) H4 cells were either untreated (Ctrl) or exposed to monomeric (M), oligomeric (O), and fibrillar (F) aSyn. (a) Lysosomal cathepsin D activity decreases significantly in oligomer- or fibril-exposed cells. (b) WB analysis of ALP markers LC3-II and p62 reveals a significant increase in LC3-II levels in aSyn-exposed cells and p62 up-regulation without reaching statistical significance. (c) H4 cells were either untreated (Ctrl), exposed to 1 µM Aβ monomers (Aβ-M), or Aβ aggregates. LC3-II levels do not change, whereas an up-regulation of p62 is measured without reaching statistical significance. Values are normalized to β-actin. WB bands for LC3-I/II, p62, and β-actin are derived from the same blot (quantification in (a,b), n = 3 and in (c), n = 4, One-way ANOVA with Tukey’s multiple comparisons tests).