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The gut microbiota has been demonstrated to play a critical role in maintaining cognitive function via the gut-brain axis, which may be related to the parasympathetic nervous system (PNS). However, the exact mechanism remains to be determined. We investigated that patients with mild cognitive impairment (MCI) and Alzheimer’s disease (AD) could exhibit an altered gut microbiota through the suppression of the PNS, compared to the healthy individuals, using the combined gut microbiota data from previous human studies. The hypothesis was validated in rats to suppress the PNS by scopolamine injections. The human fecal bacterial FASTA/Q files were selected and combined from four different AD studies (n = 410). All rats had a high-fat diet and treatments for six weeks. The MD rats had memory impairment by scopolamine injection (2 mg/kg body weight; MD, Control) or no memory impairment by saline injection. The scopolamine-injected rats had a donepezil intake as the positive group. In the optimal model generated from the XGboost analysis, <i>Blautia luti, Pseudomonas mucidoiens, Escherichia marmotae,</i> and <i>Gemmiger formicillis</i> showed a positive correlation with MCI while <i>Escherichia fergusonii</i>, <i>Mycobacterium neglectum,</i> and <i>Lawsonibacter asaccharolyticus</i> were positively correlated with AD in the participants with enterotype Bacteroides (ET-B, n = 369). The predominant bacteria in the AD group were negatively associated in the networking analysis with the bacteria in the healthy group of ET-B participants. From the animal study, the relative abundance of <i>Bacteroides</i> and <i>Bilophilia</i> was lower, and that of <i>Escherichia</i>, <i>Blautia</i>, and <i>Clostridium</i> was higher in the scopolamine-induced memory deficit (MD) group than in the normal group. These results suggest that MCI was associated with the PNS suppression and could progress to AD by exacerbating the gut dysbiosis. MCI increased <i>Clostridium</i> and <i>Blautia,</i> and its progression to AD elevated <i>Escherichia</i> and <i>Pseudomonas</i>. Therefore, the modulation of the PNS might be linked to an altered gut microbiota and brain function, potentially through the gut-brain axis.