Preprint Advancing Digital Precision Medicine for Chronic Fatigue Syndrome through Longitudinal Large-Scale Multi-Modal Biological Omics Modeling... 2025 Xiong

Andy

Senior Member (Voting rights)
Full title: Advancing Digital Precision Medicine for Chronic Fatigue Syndrome through Longitudinal Large-Scale Multi-Modal Biological Omics Modeling with Machine Learning and Artificial Intelligence

We studied a generalized question: chronic diseases like ME/CFS and long COVID exhibit high heterogeneity with multifactorial etiology and progression, complicating diagnosis and treatment. To address this, we developed BioMapAI, an explainable Deep Learning framework using the richest longitudinal multi-omics dataset for ME/CFS to date.

This dataset includes gut metagenomics, plasma metabolome, immune profiling, blood labs, and clinical symptoms. By connecting multi-omics to a symptom matrix, BioMapAI identified both disease- and symptom-specific biomarkers, reconstructed symptoms, and achieved state-of-the-art precision in disease classification. We also created the first connectivity map of these omics in both healthy and disease states and revealed how microbiome-immune-metabolome crosstalk shifted from healthy to ME/CFS.

Open access
 
To explore the generalizability of our findings, we compared our findings with those identified in 1) an additional timepoint for our current cohort: we collected metagenomics and metabolomics data again ~one year after their initial recruitment (n=107 patients, n=59 controls); 2) two independent cohorts: the microbiome cohort from Guo et al., 2023 87 with 197 long-term participants (n=106 patients, n=91 controls) and the metabolome cohort from Germain et al., 2020 69 with 56 female individuals (n=26 patients, n=26 controls).

Deficient butyrate-producing capacity in the gut microbiome is associated with bacterial network disturbances and fatigue symptoms in ME/CFS (2023)

Comprehensive Circulatory Metabolomics in ME/CFS Reveals Disrupted Metabolism of Acyl Lipids and Steroids (2020)

While there are notable biological differences in study design (e.g., long-term patients only vs. our short- and long-term cohort, gender), we found that the main conclusions and the identified biomarkers in ME/CFS were largely shared across all cohorts, supporting the robustness of our models and the validity of our findings.
 
'our team previously showed a striking immune dysbiosis in
different blood immune markers, including changes in the functional capacity of mucosal
associated invariant T (MAIT) cells and Th17 cells, and a decrease in the frequency of
CD8+ T cells and natural killer cells in long-term ME/CFS patients'

From the PDF - does anyone knkw what study this was?
 
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