Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder, primarily affecting dopaminergic neurons within the substantia nigra pars compacta. This neuronal disruption leads to a range of motor and non-motor symptoms, including tremors, bradykinesia, muscle rigidity, and, in some cases, dementia. While a small percentage of the cases are associated with genetic mutations, the majority of cases occur sporadically, implicating various biological pathways that remain to be fully explored. Neurodegeneration involves complex various biological mechanisms and agents, such as mitochondria, glial cells and neurons. Within this process, a specific microglial receptor protein, Six-Microns-under (SIMU), has captured our attention. Previous RNA sequencing data from parkin null mutant flies, a well-established model for neurodegeneration, revealed that this gene is upregulated, though its implication in PD remains unclear. Therefore, by using Drosophila melanogaster as a model, we aim to investigate its involvement in the disease. Simu is usually expressed in fly embryos with markedly reduced expression in adult flies, suggesting a role for this receptor in neuron development and regulation. Here, we will investigate SIMU protein expression in adult fly brains, its regulation by Parkin, and its physiological role. To address our questions, we will quantify simu expression and examine the localization of its product by confocal microscopy and immunostaining. Interestingly, our findings indicate no direct correlation between simu expression and hemocyte recruitment in the adult Drosophila brain. Notably, simu appears to localize predominantly around the brain rather than within its tissue. Park1 mutant flies exhibit a locomotor deficit, which is exacerbated in the double mutant park1 simu. In this work, we also show that flies expressing RNAi against SIMU also display a locomotor deficit, although the effect is less pronounced than in the simu mutant.