title: LRRK2 mutations and neurotoxicant susceptibility.
abstract: Interactions between genetic and environmental factors are thought to contribute to the pathogenesis of the majority of Parkinson's disease (PD) cases. However, our understanding of these interactions is at an early stage. Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common cause of hereditary PD. Penetrance of LRRK2 mutations is incomplete and variable, suggesting that other environmental or genetic factors may contribute to the development of the disorder. Recently, using animal models, several attempts have been made to understand if LRRK2 may mediate sensitivity to environmental neurotoxicants. Here, we critically review the most current data on how LRRK2 mutations influence neurotoxicity in PD models.
authors.affiliation: School of Health Sciences, Purdue University, West Lafayette, IN 47907, USA.
authors.forename: Jang-Won
authors.initials: JW
authors.lastname: Lee
authors.affiliation: School of Health Sciences, Purdue University, West Lafayette, IN 47907, USA cannonjr@purdue.edu.
authors.forename: Jason R
authors.initials: JR
authors.lastname: Cannon
mesh_terms: D000818:Animals; D059647:Gene-Environment Interaction; D020022:Genetic Predisposition to Disease; D006801:Humans; D000071158:Leucine-Rich Repeat Serine-Threonine Protein Kinase-2; D009154:Mutation; D009498:Neurotoxins / Q000633:toxicity*; D010302:Parkinson Disease, Secondary / Q000139:chemically induced / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D017346:Protein Serine-Threonine Kinases / Q000235:genetics* / Q000378:metabolism
chemical_list: D009498:Neurotoxins; C495280:LRRK2 protein, human; D000071158:Leucine-Rich Repeat Serine-Threonine Protein Kinase-2; D017346:Protein Serine-Threonine Kinases
keywords: Parkinson’s disease; gene–environment interaction; leucine-rich repeat kinase 2