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Commentary
Nature Cell Biology  2, E115 - E119 (2000)
doi:10.1038/35017124

Is there a cause-and-effect relationship between alpha-synuclein fibrillization and Parkinson's disease?

Matthew S. Goldberg & Peter T. Lansbury Jr

Matthew S. Goldberg and Peter T. Lansbury Jr are at the Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, The Department of Neurology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA

Correspondence should be addressed to Peter T. Lansbury Jr lansbury@cnd.bwh.harvard.edu
The first gene to be linked to Parkinson's disease encodes the neuronal protein alpha-synuclein. Recent mouse and Drosophila models of Parkinson's disease support a central role for the process of alpha-synuclein fibrillization in pathogenesis. However, some evidence indicates that the fibril itself may not be the pathogenic species. Our own biophysical studies suggest that a structured fibrillization intermediate or an alternatively assembled oligomer may be responsible for neuronal death. This speculation can now be experimentally tested in the animal models. Such experiments will have implications for the development of new therapies for Parkinson's disease and related neurodegenerative diseases.

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Nature Cell Biology
ISSN: 1465-7392
EISSN: 1476-4679
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