title: LRRK2 and neuroinflammation: partners in crime in Parkinson's disease?
abstract: It is now well established that chronic inflammation is a prominent feature of several neurodegenerative disorders including Parkinson's disease (PD). Growing evidence indicates that neuroinflammation can contribute greatly to dopaminergic neuron degeneration and progression of the disease. Recent literature highlights that leucine-rich repeat kinase 2 (LRRK2), a kinase mutated in both autosomal-dominantly inherited and sporadic PD cases, modulates inflammation in response to different pathological stimuli. In this review, we outline the state of the art of LRRK2 functions in microglia cells and in neuroinflammation. Furthermore, we discuss the potential role of LRRK2 in cytoskeleton remodeling and vesicle trafficking in microglia cells under physiological and pathological conditions. We also hypothesize that LRRK2 mutations might sensitize microglia cells toward a pro-inflammatory state, which in turn results in exacerbated inflammation with consequent neurodegeneration.
authors.affiliation: Department of Biology, University of Padova, Via Ugo Bassi 58/B, 35121 Pad ova, Italy. isabella.russo@unipd.it.
authors.forename: Isabella
authors.initials: I
authors.lastname: Russo
authors.forename: Luigi
authors.initials: L
authors.lastname: Bubacco
authors.forename: Elisa
authors.initials: E
authors.lastname: Greggio
mesh_terms: D000818:Animals; D004660:Encephalitis / Q000150:complications*; D006801:Humans; D000071158:Leucine-Rich Repeat Serine-Threonine Protein Kinase-2; D010300:Parkinson Disease / Q000150:complications* / Q000235:genetics*; D017346:Protein Serine-Threonine Kinases / Q000235:genetics*
chemical_list: C495280:LRRK2 protein, human; D000071158:Leucine-Rich Repeat Serine-Threonine Protein Kinase-2; D017346:Protein Serine-Threonine Kinases