Leucine-rich repeat kinase 2 (LRRK2), a gene linked to autoso-mal-dominantly inherited and sporadic Parkinson’s disease (PD) as a risk factor, encodes a large and complex protein with a dual enzymatic activity. LRRK2 contains several domains involved in protein-protein interactions, however, the presence of both a kinase and GTPase domain points to intracellular signaling functions (Marín, 2006). While LRRK2 has been linked to sev-eral molecular pathways important for neuronal activity (Martin et al., 2014), the observation that its expression is high in mi-croglia has attracted the attention of different groups to under-stand whether LRRK2 dysfunctions in these cells may impact neuronal activity as secondary event. In this regard, since 2012 numerous studies have demonstrated that LRRK2 controls mi-croglia activation and plays important roles in these cells (Rus-so et al., 2014). Microglia are highly specialized macrophages responsible for mediating innate immune defense in the brain and scavenging debris or misfolded/aggregated proteins. They are considered main actors upon an inflammatory stimulus, and although a well-regulated inflammatory response is crucial for tissue repair and brain homeostasis, an excessive and prolonged neuroinflammation can lead to overproduction of toxic mole-cules, which results in deleterious cellular damage, as observed in different neurodegenerative diseases including PD (Tansey and Goldberg, 2010).