Altered Gut Microbiota and Its Clinical Relevance in Mild Cognitive Impairment and Alzheimer's Disease: Shanghai Aging Study and Shanghai Memory Study

Altered gut microbiota has been reported in individuals with mild cognitive impairment (MCI) and Alzheimer's disease (AD). Previous research has suggested that specific bacterial species might be associated with the decline of cognitive function. However, the evidence was insufficient, and the results were inconsistent. To determine whether there is an alteration of gut microbiota in patients with MCI and AD and to investigate its correlation with clinical characteristics, the fecal samples from 94 cognitively normal controls (NC), 125 participants with MCI, and 83 patients with AD were collected and analyzed by 16S ribosomal RNA sequencing. The overall microbial compositions and specific taxa were compared. The clinical relevance was analyzed. There was no significant overall difference in the alpha and beta diversity among the three groups. Patients with AD or MCI had increased bacterial taxa including Erysipelatoclostridiaceae, Erysipelotrichales, Patescibacteria, Saccharimonadales, and Saccharimonadia, compared with NC group (p < 0.05), which were positively correlated with APOE 4 carrier status and Clinical Dementia Rating (correlation coefficient: 0.11 similar to 0.31, p < 0.05), and negatively associated with memory (correlation coefficient: -0.19 similar to-0.16, p < 0.01). Our results supported the hypothesis that intestinal microorganisms change in MCI and AD. The alteration in specific taxa correlated closely with clinical manifestations, indicating the potential role in AD pathogenesis.

Automated summary

Altered gut microbiota has been found in individuals with mild cognitive impairment (MCI) and Alzheimer's disease (AD). Specific bacterial taxa were increased in AD or MCI patients compared to controls, and these changes were correlated with APOE 4 carrier status, clinical dementia rating, and memory. The results suggest a potential role of gut microbiota in AD pathogenesis.