Parkinson's Disease and Related α-Synucleinopathies Are Brain Amyloidoses

Authors

  • JOHN Q. TROJANOWSKI,

    Corresponding author
    1. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, and the Institute on Aging, the University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
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  • VIRGINIA M-Y. LEE

    1. Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, and the Institute on Aging, the University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
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Address for correspondence: John Q. Trojanowski, M.D., Ph.D., Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, HUP, Maloney Building, 3rd Floor, Philadelphia, PA 19104. Voice: 215-662-6399/6427; fax: 215-349-5909. trojanow@mail.med.upenn.edu

Abstract

Abstract: A paradigm shift in understanding Parkinson's disease (PD) and related disorders is emerging from studies showing that alpha-synuclein (AS) gene mutations cause familial PD; AS is abnormally nitrated, phosphorylated, and ubiquitinated; AS forms neuronal and glial inclusions; AS fibrillizes in vitro; and AS transgenic animals develop neurodegeneration with AS amyloid inclusions. Thus, PD and related synucleinopathies are brain amyloidoses that may share similar mechanisms and targets for drug discovery.

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