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The VPS35 gene and Parkinson's disease

Authors

  • Hao Deng MD, PhD,

    Corresponding author
    1. Department of Neurology, the Third Xiangya Hospital, Central South University, Changsha, China
    • Center for Experimental Medicine, the Third Xiangya Hospital, Central South University, Changsha, China
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    • Hao Deng and Kai Gao contributed equally to this work.

  • Kai Gao MD,

    1. Center for Experimental Medicine, the Third Xiangya Hospital, Central South University, Changsha, China
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    • Hao Deng and Kai Gao contributed equally to this work.

  • Joseph Jankovic MD

    1. Department of Neurology, Baylor College of Medicine, Houston, Texas, USA
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  • Relevant conflicts of interest/financial disclosures: Hao Deng was funded by National Natural Science Foundation of China (81271921, 81101339), Sheng Hua Scholars Program of Central South University, China (H.D.), the Fundamental Research Funds for the Central Universities (2011JQ014), Research Fund for the Doctoral Program of Higher Education of China (20110162110026), and Construction Fund for Key Subjects of the Third Xiangya Hospital, Central South University. Kai Gao was supported by the Fundamental Research Funds for the Central Universities of Central South University (2012zzts120). Joseph Jankovic also receives support from the National Parkinson Foundation.

  • Full financial disclosures and author roles may be found in the online version of this article.

Correspondence to: Dr. Hao Deng, Professor of Center for Experimental Medicine and Professor of Neurology, Vice Director of Center for Experimental Medicine, the Third Xiangya Hospital, Central South University, 138 Tongzipo Road, Changsha, Hunan 410013, China; hdeng008@yahoo.com

ABSTRACT

Parkinson's disease (PD), the second most common age-related neurodegenerative disease, is characterized by loss of dopaminergic and nondopaminergic neurons, leading to a variety of motor and nonmotor symptoms. In addition to environmental factors, genetic predisposition and specific gene mutations have been shown to play an important role in the pathogenesis of this disorder. Recently, the identification of the vacuolar protein sorting 35 homolog gene (VPS35), linked to autosomal dominant late-onset PD, has provided new clues to the pathogenesis of PD. Here we discuss the VPS35 gene, its protein function, and various pathways involved in Wnt/β-catenin signaling and in the role of DMT1 mediating the uptake of iron and iron translocation from endosomes to the cytoplasm. Further understanding of these mechanisms will undoubtedly provide new insights into the pathogenic mechanisms of PD and may lead to prevention and better treatment of the disorder. © 2013 Movement Disorder Society

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