Microbiome-targeted strategies for Alzheimer’s disease: multi-omics signatures, mechanistic links, and intervention evidence
- 1Department of Neurology, Central Hospital Affiliated to Shenyang Medical College
- 2Department of Pediatrics, Liaoning Provincial People’s Hospital
- 3Department of Emergency, Central Hospital Affiliated to Shenyang Medical College
Abstract
Alzheimer’s disease (AD) is increasingly studied in relation to gut microbial mechanisms because microbial metabolism, mucosal barrier function, and peripheral immune activation may influence neuroinflammation and host metabolic stress. This review evaluates microbiome-linked evidence in AD with emphasis on studies that combine metagenomics, metabolomics, inflammatory markers, neuroimaging, cerebrospinal fluid or blood biomarkers, and cognitive phenotyping. Current data support several recurring but not yet causal axes, including bile acid transformation, short-chain fatty acid (SCFA) production, trimethylamine N-oxide (TMAO), bacterial product-related inflammatory signaling, and barrier dysfunction. We also review microbiome-targeted interventions, including diet and prebiotics, strain-specified probiotics and synbiotics, oligosaccharide-based agents, gut-restricted antimicrobials, and fecal microbiota transplantation (FMT). The strength of evidence differs substantially across these strategies: sodium oligomannate has been tested in a phase 3 trial, whereas many probiotic, antimicrobial, and FMT approaches remain early clinical, preclinical, or mechanism-generating. Future trials should define a priori microbial, metabolite, immune, and brain biomarker endpoints; control diet, medication, and comorbidity confounding; and validate candidate signatures across independent cohorts before using microbiome profiles for screening or treatment selection.
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BibTeX
@article{huang2026microbiometargeted,
title = {{Microbiome-targeted strategies for Alzheimer’s disease: multi-omics signatures, mechanistic links, and intervention evidence}},
author = {Xuyang Huang and Xinyue Zhang and Qi Zhu},
journal = {Frontiers in Microbiology},
year = {2026},
month = oct,
doi = {10.3389/fmicb.2026.1828118},
url = {https://www.frontiersin.org/articles/10.3389/fmicb.2026.1828118/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Microbiome-targeted strategies for Alzheimer’s disease: multi-omics signatures, mechanistic links, and intervention evidence
AU - Xuyang Huang
AU - Xinyue Zhang
AU - Qi Zhu
PY - 2026
DA - 2026/10/28
JO - Frontiers in Microbiology
DO - 10.3389/fmicb.2026.1828118
UR - https://www.frontiersin.org/articles/10.3389/fmicb.2026.1828118/full
AB - Alzheimer’s disease (AD) is increasingly studied in relation to gut microbial mechanisms because microbial metabolism, mucosal barrier function, and peripheral immune activation may influence neuroinflammation and host metabolic stress. This review evaluates microbiome-linked evidence in AD with emphasis on studies that combine metagenomics, metabolomics, inflammatory markers, neuroimaging, cerebrospinal fluid or blood biomarkers, and cognitive phenotyping. Current data support several recurring but not yet causal axes, including bile acid transformation, short-chain fatty acid (SCFA) production, trimethylamine N-oxide (TMAO), bacterial product-related inflammatory signaling, and barrier dysfunction. We also review microbiome-targeted interventions, including diet and prebiotics, strain-specified probiotics and synbiotics, oligosaccharide-based agents, gut-restricted antimicrobials, and fecal microbiota transplantation (FMT). The strength of evidence differs substantially across these strategies: sodium oligomannate has been tested in a phase 3 trial, whereas many probiotic, antimicrobial, and FMT approaches remain early clinical, preclinical, or mechanism-generating. Future trials should define a priori microbial, metabolite, immune, and brain biomarker endpoints; control diet, medication, and comorbidity confounding; and validate candidate signatures across independent cohorts before using microbiome profiles for screening or treatment selection.
SN - 1664-302X
ER -