iScienceJul 28, 2026

Gut microbiome patterns linked to memory loss in Alzheimer's disease revealed by multi-omics analysis

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗

Updated Aug 3, 2026

Abstract

Distinct microbial community structures and altered metabolic profiles were observed in 28 patients with Alzheimer's disease compared to 33 controls.

Increased abundance of Akkermansia massiliensis, Alistipes onderdonkii, and Barnesiella intestinihominis was found in patients with Alzheimer's disease.
Phageome analysis showed a greater richness of Podoviridae and a decrease in Microviridae in the Alzheimer's group.
Shifts in microbial metabolic pathways related to tryptophan and short-chain fatty acid metabolism were identified.
Elevated levels of fecal spermidine, taurocholate, and glycerophosphocholine were detected in Alzheimer's patients.
A classification model based on metabolites and gut microbial data achieved an area under the curve (AUC) of 0.83 for within-cohort classification.

Simplified

Alzheimer's disease (AD) is increasingly being linked to gut microbial dysbiosis via the gut-brain axis. We applied integrated metagenomics and metabolomics to characterize gut microecology in 28 patients with AD and 33 controls. Metagenomic analysis revealed distinct microbial community structures, with increased abundance of Akkermansia massiliensis, Alistipes onderdonkii, and Barnesiella intestinihominis in AD. Phageome analysis revealed increased richness and altered composition, with more Podoviridae and fewer Microviridae. Functional profiling identified shifts in microbial metabolic pathways involving tryptophan and short-chain fatty acid metabolism. Untargeted metabolomics revealed elevated fecal spermidine, taurocholate, and glycerophosphocholine levels in patients with AD. A random forest model combining metabolites, gut metabolic modules, and bacteriophages achieved good within-cohort classification (AUC = 0.83) but lacked external validation due to unavailable matched fecal metabolomic data. Overall, these findings link AD to coordinated disruptions across bacterial, viral, and metabolic gut layers, highlighting the need for external validation and mechanistic studies.