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Mutations in the LRRK2 (leucine-rich repeat kinase 2) gene on chromosome 12 cause autosomal dominant PD (Parkinson's disease), which is indistinguishable from sporadic forms of the disease. Numerous attempts have therefore been made to model PD in rodents via the transgenic expression of LRRK2 and its mutant variants and to elucidate the function of LRRK2 by knocking out rodent Lrrk2. Although these models often only partially recapitulate PD pathology, they have helped to elucidate both the normal and pathological function of LRRK2. In particular, LRRK2 has been suggested to play roles in cytoskeletal dynamics, synaptic machinery, dopamine homoeostasis and autophagic processes. Our understanding of how these pathways are affected, their contribution towards PD development and their interaction with one another is still incomplete, however. The present review summarizes the findings from LRRK2 rodent models and draws potential connections between the apparently disparate cellular processes altered, in order to better understand the underlying mechanisms of LRRK2 dysfunction and illuminate future therapeutic interventions.

Original publication

DOI

10.1042/BST20120151

Type

Journal article

Journal

Biochem Soc Trans

Publication Date

10/2012

Volume

40

Pages

1080 - 1085

Keywords

Animals, Disease Models, Animal, Gene Deletion, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Mice, Mice, Knockout, Mice, Transgenic, Parkinson Disease, Protein-Serine-Threonine Kinases