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. 2020 Aug 4;10:13149. doi: 10.1038/s41598-020-70174-z

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© The Author(s) 2020

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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Autophagic-lysosomal pathway in PD. Autophagic and lysosomal markers were determined in post-mortem human brain samples from SNpc, Hippocampus and Cortex of sporadic PD patients and controls. The levels of LC3II, p62, Beclin1, Lamp2A, Lamp1 and CatD were determined in: (A) SNpc; (B) Hippocampus and (C) Cortex brain tissue homogenates. (D) Densitometric analysis of the levels of LC3II, p62, Beclin1, Lamp2A, Lamp1 and CatD. The blots were re-probed for α-tubulin to confirm equal protein loading Values are mean ± SEM (n = 5, **p < 0.01, versus SNpc control subjects; ^###p < 0.001, versus hippocampus control subjects and ^&&p < 0. 01, versus cortex control subjects). Full length blots are presented in the Supplementary Information.