title: Inflammation is genetically implicated in Parkinson's disease.
abstract: Inflammation has long been associated with the pathogenesis of Parkinson's disease (PD) but the extent to which it is a cause or consequence is sill debated. Over the past decade a number of genes have been implicated in PD. Relatively rare missense mutations in genes such as LRRK2, Parkin, SNCA and PINK1 are causative for familial PD whereas more common variation in genes, including LRRK2, SNCA and GBA, comprise risk factors for sporadic PD. Determining how the function of these genes and the proteins they encode are altered in PD has become a priority, as results will likely provide much needed insights into contributing causes. Accumulating evidence indicates that many of these genes function in pathways that regulate aspects of immunity, particularly inflammation, suggesting close associations between PD and immune homeostasis.
authors.affiliation: School of Medical Sciences, University of NSW, Sydney, NSW 2052, Australia; Neuroscience Research Australia, Randwick, NSW 2031, Australia. Electronic address: n.dzamko@neura.edu.au.
authors.forename: N
authors.initials: N
authors.lastname: Dzamko
authors.affiliation: School of Medical Sciences, University of NSW, Sydney, NSW 2052, Australia.
authors.forename: C L
authors.initials: CL
authors.lastname: Geczy
authors.affiliation: School of Medical Sciences, University of NSW, Sydney, NSW 2052, Australia; Neuroscience Research Australia, Randwick, NSW 2031, Australia. Electronic address: g.halliday@neura.edu.au.
authors.forename: G M
authors.initials: GM
authors.lastname: Halliday
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000209:etiology* / Q000235:genetics*; D010300:Parkinson Disease / Q000150:complications* / Q000235:genetics*; D017382:Reactive Oxygen Species / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D016207:Cytokines; D017382:Reactive Oxygen Species; D051193:Toll-Like Receptors
keywords: LRRK2; TLR; inflammation; innate; parkin; synuclein