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

Guoxiang Liu, Leonardo Aliaga, Huaibin Cai

    Research output: Contribution to journalReview articlepeer-review

    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the pathophysiological functions of α-syn, LRRK2 and their interaction in PD, based on the available literature and our unpublished observations.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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