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. 2022 Mar 21;12:4797. doi: 10.1038/s41598-022-08840-7

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© The Author(s) 2022

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/.

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Peripheral impact of CRL treatment. A Quantification of immune cell population by flow cytometry analysis. No difference was observed in CD4+CD3+, CD8+CD3+ and their ratio, respectively. B Peripheral inflammation measured by plasma cytokine and chemokine levels. No biologically-relevant significant changes could be determined. C Pathway analysis of untargeted plasma metabolomics data indicating significant changes in UFA and glycerophospholipid metabolism. D Investigation of subclasses of UFA, SFA and UFA/SFA revealed an UFA specific elevation in APP/PS1 mice and reduction post treatment. E ω-3 and ω-6 fatty acid levels measured in plasma. All subtypes showed significant or trending normalization of UFA level post CRL treatment in APP/PS1 mice. F HDL and VLDL/LDL cholesterol and cholesterol esters to analyze CRL’s effect on lipid transport. VLDL/LDL cholesterol and cholesterol ester fraction were both significantly increased. Significance was assessed by 2-way ANOVA and post-hoc Tukey correction. Significance: *p < 0.05, **p < 0.01, ***p < 0.001.