Parkinson’s Disease (PD) is the fastest growing neurodegenerative disease and manifests as a synucleinopathy with reduced motor output. Non-motor symptoms often precede or coincide with the hallmark motor symptoms in PD. Multiple studies have identified altered gut-microbial composition in PD, but the underlying pathological and function significance of these changes remains unknown. In this study, we identified the changes in the gut-microbial composition relevant to PD in an α-synuclein transgenic mouse model of PD at early and late stages of the disease. M83-transgenic mice express the full length A53T human-α-synuclein variant, making it an excellent model to study PD-synuclein pathology. We utilised high-resolution functional metagenomics with ultra-deep sequencing to ensure identification of low-abundance and novel taxa. The microbial community and metabolic pathways were profiled using Microba community and pathway profiler respectively. Although the microbial alpha-diversity remained unchanged in the M83 transgenic and WT group across different stages of PD a difference in microbial composition was observed. M83-transgenics occupied two separate clusters across both the stages of the disease. Gut dysbiosis in the early stages of PD was characterised with an increase in Staphylococcus, Hungatella, and kineothrix species and a decrease of Duncaniella and Muribaculum species. A decrease in genera lactobacillus was observed in later stages of PD. Microbes associated with blood-glucose levels, metabolic inflammation, SCFA production decreased whereas butyrate producers and opportunistic pathogens increased in abundance in our dataset. Our results provide evidence to support the hypothesis that the gut-microbial changes could contribute to the onset and progression of PD.