A group of researchers evaluated human evidence examining how alterations in the gut microbiome are associated with mild cognitive impairment (MCI) and Alzheimer’s disease (AD).
Study
A scoping review methodology was applied using the five-stage framework proposed by Arksey and O’Malley and guided by the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews (PRISMA-ScR) checklist. Researchers searched PubMed, Scopus, and the Cochrane Library up to February 2023 for studies examining the gut microbiome in individuals with MCI or AD. Eligible publications included original research articles, systematic reviews, and meta-analyses.
Animal studies, non-English literature, and studies that did not directly evaluate gut microbiota composition were excluded. Multiple reviewers independently screened titles and abstracts, and studies meeting predefined inclusion and exclusion criteria were assessed at the full-text level.
Data were extracted on participant characteristics, microbiome assessment methods, cognitive outcomes, and key findings. Quantitative synthesis was not performed due to substantial methodological heterogeneity, including variation in sequencing techniques, dietary assessments, and cognitive testing. Instead, results were summarized narratively, highlighting recurrent microbial patterns, diversity metrics, and cognitive associations reported across observational and interventional studies.
Findings
Overall, the evidence indicated recurrent but heterogeneous differences in gut microbiota composition between individuals with MCI or AD and cognitively normal controls, with limited overlap in specific taxa reported across independent cohorts.
Several observational studies linked AD to gut dysbiosis, with many reporting reduced microbial diversity, although this finding was not universal. In contrast, alpha-diversity differences were less consistently observed in MCI. Individuals with AD were more frequently reported to have higher relative abundances of potentially pathogenic taxa such as Pseudomonadota and Actinomycetota.
Findings in MCI were more variable. Some studies reported increased abundance of short-chain fatty acid-producing genera such as Faecalibacterium and Roseburia, while others observed reductions in these same taxa. These inconsistencies were often noted in small, population-specific studies, underscoring limited reproducibility across cohorts.
At the species level, Escherichia coli was the only microorganism repeatedly identified as elevated across multiple AD studies, suggesting a potential role in inflammation or metabolic dysregulation. In contrast, fiber-fermenting and butyrate-producing genera such as Ruminococcus, Parabacteroides, and Butyricicoccus were more frequently reported in cognitively healthy controls, although these associations were inconsistent across studies.
Conclusion
Human evidence increasingly supports an association between gut microbiome alterations and cognitive decline across the Alzheimer’s disease spectrum. Changes in microbial diversity and composition appear to occur in subsets of individuals during early MCI and persist throughout AD progression, potentially influencing neuroinflammatory pathways and brain health. Because the gut microbiome is modifiable through diet, probiotics, and lifestyle factors, these findings raise theoretical opportunities for risk modification.
However, substantial methodological variability, limited longitudinal data, and a predominant focus on microbial composition rather than functional or metabolic profiling preclude causal inference. Further well-designed human studies and long-term intervention trials are required to determine whether targeting the gut microbiome can meaningfully alter the trajectory of cognitive aging and Alzheimer’s disease.
Source:
https://www.news-medical.net/news/20260125/Evidence-links-gut-microbiome-changes-to-Alzheimere28099s-progression.aspx