Models of LRRK2-associated parkinson’s disease

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common genetic causes of Parkinson’s disease (PD) and also one of the strongest genetic risk factors in sporadic PD. The LRRK2 protein contains a GTPase and a kinase domain and several protein-protein interaction domains. Both in vitro and in vivo assays in different model systems have provided tremendous insights into the molecular mechanisms underlying LRRK2-induced dopaminergic neurodegeneration. Among all the model systems, animal models are crucial tools to study the pathogenesis of human disease. How do the animal models recapitulate LRRK2-induced dopaminergic neuronal loss in human PD? To answer this question, this review focuses on the discussion of the animal models of LRRK2-associated PD including genetic-and viral-based models.

Original languageEnglish (US)
Title of host publicationAdvances in Neurobiology
PublisherSpringer New York LLC
Pages163-191
Number of pages29
Volume14
DOIs
StatePublished - Apr 1 2017

Publication series

NameAdvances in Neurobiology
Volume14
ISSN (Print)21905215

    Fingerprint

Keywords

  • Animal models
  • LRRK2
  • Parkinson’s disease

ASJC Scopus subject areas

  • Biochemistry
  • Neurology
  • Developmental Neuroscience
  • Cellular and Molecular Neuroscience

Cite this

Xiong, Y., Dawson, T. M., & Dawson, V. (2017). Models of LRRK2-associated parkinson’s disease. In Advances in Neurobiology (Vol. 14, pp. 163-191). (Advances in Neurobiology; Vol. 14). Springer New York LLC. https://doi.org/10.1007/978-3-319-49969-7_9