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. 2023 May 16;20:116. doi: 10.1186/s12974-023-02802-0

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — miRNAs that target autophagy and dopamine metabolism are significantly altered between placebo and nilotinib. A total of 17 microRNAs (1.6%) were significantly different between the placebo and nilotinib groups, accounting for both treatment and time. Ingenuity Pathway Analysis of microRNA matched associated mRNAs or targets that are experimentally validated from TarBase, miRecords, as well as highly predicted miRNA–mRNA interactions from TargetScan and revealed that 14 of these microRNAs are associated with genes that control autophagy and dopamine metabolism. N = 11 placebo, n = 12 nilotinib