A research review published in Alzheimer’s & Dementia summarizes current human evidence linking changes in the gut microbiome to mild cognitive impairment (MCI) and Alzheimer’s disease (AD). The review clarifies what is currently known about microbiota changes across the cognitive impairment spectrum and how these findings may inform future diagnostic approaches.
The authors analyzed 58 human studies, including observational studies, clinical trials, systematic reviews, and meta-analyses. Most studies used 16S ribosomal RNA sequencing to characterize gut bacteria, with fewer assessing microbial function or metabolites. Animal studies were excluded to focus on findings directly relevant to human disease.
Across studies, individuals with MCI or AD frequently showed differences in gut microbiota compared with cognitively healthy controls. However, patterns varied between disease stages. In MCI, several studies reported higher abundance of bacteria such as Faecalibacterium and Roseburia, which are commonly linked to short-chain fatty acid production and gut barrier function. In contrast, AD was more consistently associated with increases in bacteria from groups such as Pseudomonadota and Actinomycetota, including Escherichia, Enterobacter, Akkermansia, and Streptococcus.
Measures of microbial diversity showed mixed results. Alpha diversity was often similar between individuals with MCI and controls but tended to be lower in AD. Beta diversity analyses more consistently showed distinct microbial community profiles in people with cognitive impairment. At the species level, Escherichia coli was the only organism repeatedly reported as increased in AD across multiple studies.
Several studies examined associations between gut microbiota and established biomarkers of AD. Altered microbial profiles were linked to changes in cerebrospinal fluid amyloid-β and phosphorylated tau levels, as well as markers of inflammation. Functional analyses suggested reduced microbial pathways related to immune regulation and energy metabolism in AD, findings that may be relevant to disease mechanisms.
Intervention studies included probiotics, dietary changes, and lifestyle interventions. Some reported modest cognitive improvements alongside microbiome changes, but results were inconsistent and limited by small sample sizes and short follow-up periods.
This review highlights both interest and limitations. While certain microbial patterns appear repeatedly, differences in study design, populations, sequencing methods, and reporting make it difficult to compare results or define reliable biomarkers. The authors note that standardized sampling, longitudinal studies, and integration of microbiome data with existing biomarkers will be needed before microbiome-based approaches can be considered for clinical use.
