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. 2024 Oct 10;12:160. doi: 10.1186/s40478-024-01864-2

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 1 — Comparison of endocannabinoids and ECS-associated lipids, peptide endocannabinoids and glucocorticoids in serum and CSF between MS and control patients. (a) Graphical presentation of analytes with the molecular structure of the endocannabinoids, associated lipids and the glucocorticoids as well as the amino acid sequence of Pepcan-23 (precursor peptide) and RVD-hemopressin. (b) Fold change as median ratio of analyte levels in samples of MS patients divided by analyte levels of control (Ctrl) patients in serum and CSF presented in a heatmap. The color-coding legend of the heatmap is shown at the bottom and reaches from 0.5 (blue, indicative for reduction of MS patient analyte level to the half of the analyte level in the Ctrl patients), over 1 (white, comparable analyte levels between MS and Ctrl patients) to 2 (yellow, analyte levels are doubled in MS compared to Ctrl patients). Significant differences between analytes of MS and Ctrl patients are labelled in bold. (c) Example graphs of analytes in serum and CSF of Ctrl (n = 80) and MS (n = 74) patients. Data are presented as box plots with median and 25–75% percentile as box with the range as whiskers. The mean is additionally depicted as + and the analyte level of each patient is represented as one data point (symbol). The number of patients where an analyte level was lower than the limit of quantification (LOQ) is indicated for each group if applicable. For statistical analysis a Mann-Whitney test was performed. Statistically significant differences are indicated as follows: * p < 0.05 and ** p < 0.01. 2-AG, 2-arachidonoylglycerol; 2-OG, 2-oleoylglycerol; AA, arachidonic acid; AEA, arachidonoylethanolamide; COX, cyclooxygenase; DAGL, Diacylglycerol lipase; EtNH2, Ethanolamine; FAAH, fatty-acid amide hydrolase; LEA, linoleoylethanolamide; MAGL, Monoacylglycerol lipase; NArPE: N-arachidonoyl phosphatidylethanolamine, NAPE-PLD, N-acyl phosphatidylethanolamine phospholipase D; n.d., not detectable; OEA, oleoylethanolamide; PEA, palmitoylethanolamide; PGD2, prostaglandin D2; PGE2, prostaglandin E2; PGH2, prostaglandin H2; SAG, 1-Stearoyl-2-arachidonoyl-sn-glycerol; SEA, stearoylethanolamide