Objective A number of evidences indicate that the intestinal flora of Parkinson's disease patients is abnormal, and whether Prnp-SNCA-A53T Parkinson's disease transgenic mice also have intestinal flora dysbiosis has not been reported. Microbial ecological characteristics were analyzed.
Methods Illumina high-throughput sequencing technology was used to sequence the V3-V4 region of fecal microbial 16S rRNA gene in 7 female transgenic mice and 13 wild-type mice of the same sex and same age, and use PICRUST to predict differential functional pathways.
Results Compared with the wild-type group, the α-diversity of the intestinal microbes of the mice in the A53T group increased, and the microbial composition and species were also significantly different: the intestinal microbes in the A53T group were increased at the phylum level, and the actinomycetes phyla increased ( P = 0. 0094), Bacteroidetes decreased (P = 0. 0498); at the class level, Rhododendron increased (P < 0. 0001), Bacteroidetes decreased (P = 0. 0398); At the level of Rhodobacter (P < 0. 0001), Bacteroidetes (P = 0. 0398) and Rhodobacter decreased (P = 0. 0185); at the family level, Rhodobacter increased (P < 0. 0185). 0. 0001), Bacteroidetes (P = 0. 0277) and Rhodobacteriaceae decreased (P = 0. 0185); at the genus level, Eaglezella increased (P = 0. 0002), Bacteroides Genus (P=0.0277) and Rhodobacter (P=0.0249). In addition, there were significant differences between the A53T group and the wild-type group in 9 functional pathways, namely G protein-coupled receptors, steroid hormone synthesis, penicillin and cephalosporin biosynthesis, ubiquinone and other terpenoid quinone biosynthesis. , Biosynthesis and metabolism of toluene degradation, glycan biosynthesis and metabolism, electron transfer carriers, meiosis, and African trypanosomiasis.
Conclusion The results of this study show that the transgenic mice have intestinal flora imbalance, and there are differences in the metabolic pathways between the transgenic model mice and wild-type mice, which provides a theoretical basis for the later study of the relationship between intestinal flora and Parkinson's disease.