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. 2019 Jun 10;9:8362. doi: 10.1038/s41598-019-42847-x

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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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Delayed start GM1 administration partially protected against loss of SNc dopaminergic neurons. (A) There was a significant protective effect of delayed start GM1 administration (N = 17) on the number of TH⁺ cells (**P = 0.0013) and the number of Nissl-stained cells (B) (***P = 0.0008 vs. saline-treated) in the SNc, compared to saline-treated animals (N = 12). (C) Immunohistochemical staining of TH⁺ cells in the SNc showed significant cell loss in a saline-treated animal and (D), a partial paring of TH⁺ cells in a GM1-treated animal.