α-synuclein, LRRK2 and their interplay in Parkinson's disease

Guoxiang Liu*, Leonardo Aliaga, Huaibin Cai

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

23 Scopus citations

Abstract

Of the various genetic factors contributing to the pathogenesis of Parkinson's disease (PD), only mutations in α-synuclein (α-syn) and LRRK2 genes cause clinical and neuropathological phenotypes closely resembling the sporadic cases. Therefore, studying the pathophysiological functions of these two PD-related genes is particularly informative in understanding the underlying molecular pathogenic mechanism of the disease. PD-related missense and multiplication mutations in α-syn may cause both early- and late-onset PD, whereas various PD-related LRRK2 missense mutations may contribute to the more common late-onset PD. While intensive studies have been carried out to elucidate the pathogenic properties of PD-related mutant α-syn and LRRK2, our knowledge of their normal functions and their potential genetic interplay remains rudimental. In this review, we summarize the progress made regarding the pathophysiological functions of α-syn, LRRK2 and their interaction in PD, based on the available literature and our unpublished observations.

Original languageEnglish (US)
Pages (from-to)145-153
Number of pages9
JournalFuture Neurology
Volume7
Issue number2
DOIs
StatePublished - Mar 2012

Keywords

  • 14-3-3
  • ER
  • Golgi apparatus
  • Lewy body
  • Parkinson's disease
  • actin
  • autophagy
  • leucine-rich repeat kinase 2
  • microtubule
  • mitochondria
  • proteasome
  • α-synuclein

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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