ArticleCureus2026
Differential Causal Associations of Gut Microbiota, Blood Metabolites, and Immune Cell Phenotypes With Early- and Late-Onset Alzheimer's Disease: A Bidirectional Mendelian Randomization Analysis.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Authors and funding
3 authors.
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Abstract
backgroundAlzheimer's disease (AD) is a heterogeneous syndrome with distinct genetic and clinical profiles between early-onset AD (EOAD) and late-onset AD (LOAD) subtypes. However, specific causal etiologies linking the gut microbiota-immune-metabolic axis to these subtypes remain poorly understood.
methodsWe employed a comprehensive bidirectional two-sample Mendelian randomization (MR) framework to systematically investigate the causal associations of gut microbiota, immune cell phenotypes, and blood metabolites with EOAD and LOAD. Large-scale genome-wide association study (GWAS) summary statistics were utilized from the MiBioGen consortium, Sardinian cohort, and Canadian Longitudinal Study on Aging, alongside AD outcome data from the FinnGen consortium. Causal estimates were generated using the inverse variance-weighted method, with rigorous sensitivity analyses including false discovery rate (FDR) correction and Steiger directionality tests to ensure robustness.
resultsOur analysis revealed divergent multi-omics signatures for AD subtypes. While the genus
conclusionsThis study provides genetic evidence that EOAD and LOAD are driven by fundamentally different peripheral mechanisms across the gut-immune-metabolic axis. These findings challenge the monolithic view of AD pathogenesis and underscore the critical necessity of stratifying patients by onset age to develop precision therapeutic interventions.
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