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Additional file 9 : Table S6. Spearman's rank order correlation between AD-related markers and plasma lipid mediators. Analysis performed utilizing only subjects predicted to be fasted with the probability >60%, including 60 AD patients and 96 healthy controls. Only associations with the p

Additional file 9 : Table S6. Spearman's rank order correlation between AD-related markers and plasma lipid mediators. Analysis performed utilizing only subjects predicted to be fasted with the probability >60%, including 60 AD patients and 96 healthy controls. Only associations with the p

Additional file 1 : Figure S1. Bile acids biosynthesis pathway. Node colors represent primary (blue) and secondary (dark red) bile acids. Node shape represent conjugated (diamond) and unconjugated (oval) bile acids. Node size represents median concentration in the experimental cohort. Cholesterol (top of the pathway) is converted to primary bile acids along two pathways, neutral and acidic [1]. Further, primary bile acids are secreted to gut, and portion of it being modify by the gut bacteria to secondary bile acids. Primary and secondary bile acids are reabsorbed into the blood stream and reenter the liver, where they are conjugated with amino acids glycine or taurine. Conjugated bile acids are then being secreted back to the gut along with primary bile acids. Gut bacteria can cleave conjugated amino acids off bile acids [2], and freed metabolites are recirculated. Therefore, plasma levels of conjugated bile acids can me a reflection of both liver and gut bacteria activity. Refference: 1.Pandak, W.M. and G. Kakiyama, The acidic pathway of bile acid synthesis: Not just an alternative pathway(). Liver Res, 2019. 3(2): p. 88-98; 2. Ridlon, J.M., et al., Consequences of bile salt biotransformations by intestinal bacteria. Gut Microbes, 2016. 7(1): p. 22-39.

Additional file 3 : Figure S3. Control and AD group MoCA and log(t-Tau/Aβ42).

Additional file 2 : Figure S2. Multilinear regression of log(t-Tau/AB42) and the components of AD predictive models, presented in the Figure 4. Analysis performed separately for plasma (upper panel) and CSF (lower panel) AD predictors. Association of individual components are shown in the leverage plots, whereas effect summery contain descriptive statistics for each individual metabolite in the model.

Additional file 3 : Figure S3. Control and AD group MoCA and log(t-Tau/Aβ42).

Additional file 11 : Table S8. Stepwise logistic model predicting AD status using plasma, CSF or both plasma and CSF metabolites. Stepwise analysis was performed with the maximal validation r2 as the model stopping criteria, or if an additional step increased the BIC. Model stopping point for each analysis is highlighted.

Additional file 10 : Table S7. Spearman's rank order correlation between AD-related markers and CSF lipid mediators. Analysis performed utilizing 151 AD patients and 142 healthy controls. Only associations with the p>0.05 are displayed. Associations colored based on Spearman’s ρ (values shown in the table), with blue color for negative and orange for positive associations.

Additional file 2 : Figure S2. Multilinear regression of log(t-Tau/AB42) and the components of AD predictive models, presented in the Figure 4. Analysis performed separately for plasma (upper panel) and CSF (lower panel) AD predictors. Association of individual components are shown in the leverage plots, whereas effect summery contain descriptive statistics for each individual metabolite in the model.