Based on previous results and the importance of non-cell autonomous pathogenic mechanisms in several neurological disorders, we generated an LRRK2 Drosophila model in which the LRRK2 expression is driven by a glial promoter (Repo-GAL4) compared to a ubiquitous promoter (Actin-GAL4) or control flies. This evidence concerns the gene LRRK2 and nervous system disorder.