The role of dysregulated gut microbiota (GM) is widely recognized as relevant to the pathogenesis of Parkinson's disease (PD), particularly in case of non-motor symptoms such as depression and anhedonia. Most transgenic mouse models of PD, however, don’t exhibit clinically relevant dysbiosis. Here, for the first time, we present the GM composition and depression-like behavior in Hualpha-Syn(A53T) transgenic mice, line G2-3, which over-express human α-synuclein and are the only model of PD that exhibits prodromal constipation. Additionally, we investigated whether sharing social microenvironment affects GM and behavior of transgenic mice (Tg+) and their non-transgenic littermates (Tg-). Four groups were formed: Tg+ and Tg- mice in mixed-group housing (MGH) and single-group housing (SGH; starting from postnatal day 30). C57BL/6J mice served as additional controls. Anhedonia and depression-like behavior were assessed using the Sucrose Preference Test and Tail Suspension Test in 6-month-old animals. Fecal samples underwent 16S rRNA sequencing. Results indicate: 1) Tg+ animals display an increase of Bacteroides, Ligilactobacillus and Bifidobacterium depending on social microenvironment; 2) Tg+ animals exhibit anhedonia and depression-like behavior regardless of microenvironment; 3) Hedonic and depression-like behavior between Tg+ and Tg- mice was different only in SGH conditions; 4) α and β diversity were stable regardless of social microenvironment. This study indicates that Hualpha-Syn(A53T) transgenic line G2-3 has translational value as a model of dysbiosis, anhedonia and depression-like behavior in the pre-motor phase of PD, while also shedding light on the crucial impact of social microenvironment on the detectability of clinically relevant indicators of the disease.