Microbiota-Gut-Brain Axis in Alzheimer's Disease: Linking Oxidative Stress, Mitochondrial Dysfunction and Amyloid Pathology-A Systematic Review.
Level 5 - mechanism / opinion, no new human data
Systematic review synthesizing heterogeneous mechanistic, preclinical, and clinical literature without a meta-analysis of randomized trials.
PubMed 42072403 · doi:10.3390/biomedicines14040860
What was done
A systematic review of PubMed, Scopus, and Web of Science databases was conducted to evaluate the role of the microbiota-gut-brain axis in Alzheimer's disease (AD). The authors analyzed studies investigating gut microbial composition, metabolomics, oxidative stress markers, mitochondrial activity, and therapeutic interventions in both AD animal models and human patients.
What was found
The abstract reports no numerical data, sample sizes, or effect estimates. Qualitatively, AD is associated with increases in pro-inflammatory bacterial taxa (Escherichia-Shigella, Bacteroides) and reductions in short-chain fatty acid-producing bacteria (Faecalibacterium, Roseburia). This dysbiosis is linked to systemic inflammation, intestinal barrier disruption, microglial activation, oxidative stress, and mitochondrial impairment. Interventions with probiotics, prebiotics, and fecal microbiota transplantation were reported to improve redox balance, reduce neuroinflammation, and improve cognitive outcomes in preclinical and clinical studies.
Why it matters
This review links gut microbiome alterations directly to mitochondrial dysfunction and oxidative damage in Alzheimer's pathogenesis. It frames the microbiota-gut-brain axis as a potential target for early biomarker identification and microbiome-targeted therapeutics.
Limits
The abstract does not state the number of included studies, sample sizes, or quantitative effect sizes. Evidence is heavily reliant on preclinical animal models mixed with human data, limiting direct clinical translation without standardized, longitudinal human trials.
Cited by
- supports Changes in gut bacteria leading to intestinal permeability cause increased systemic inflammation that activates microglial cells.