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. 2022 Feb 1;14:19. doi: 10.1186/s13195-022-00966-0

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© The Author(s) 2022

Open AccessThis 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. 2 — Brain ganglioside GM3 levels in AD mice are reduced after glucosylceramide (GlcCer) synthase inhibitor (GCSi) treatment. A Overview of the glycosphingolipid pathway (Glc, glucose; LacCer, lactosylceramide; GM3, GM2 and GM1, ganglioside GM3, GM2 and GM1; UGCG, GlcCer synthase; B4galT6, LacCer synthase; B4galnt1, GM3 synthase; B3galnt1, GM2 synthase; St3gal5, GM1 synthase). B WT mice feature regional variation in GlcCer and GM3 levels in the cortex, hippocampus, and amygdala. C AD (Tg2576) mice treated with GCSi show significant reductions in GM3 levels in the amygdala and cortex. Columns not connected by the same letter are significantly (p = 0.01) different from each other. Error bars represent ± SEM