Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by McNaught, K. St. P.
Right arrow Articles by Olanow, C. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McNaught, K. St. P.
Right arrow Articles by Olanow, C. W.
NEUROLOGY 2006;66:S37-S49
© 2006 American Academy of Neurology

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology.

Proteasomal dysfunction in sporadic Parkinson's disease

Kevin St. P. McNaught, PhD, Tehone Jackson, BSc, Ruth JnoBaptiste, BA, Alexander Kapustin, PhD and C. Warren Olanow, MD, FRCPC

From the Department of Neurology, Mount Sinai School of Medicine, New York, New York.

Address correspondence and reprint requests to Dr. Kevin St. P. McNaught, Department of Neurology, Mount Sinai School of Medicine, Annenberg 14–73, One Gustave L. Levy Place, New York, NY 10029; e-mail: kevin.mcnaught{at}mssm.edu

The cause and mechanism of neuronal death in sporadic Parkinson's disease (PD) continue to elude investigators. Recently, alterations in proteasomal function have been detected in the brain of patients with the illness. The biochemical basis of the defect and its relevance to the disease process are now being studied. The available results suggest that proteasomal dysfunction could underlie protein accumulation, Lewy body formation, and neuron death in PD. The cause of proteasomal dysfunction is unknown at present, but this could relate to gene mutations, oxidative damage, ATP depletion, or the actions of environmental toxins. It remains to be established if proteasomal dysfunction plays a primary or a secondary role in the initiation or progression of the neurodegenerative process in PD.


This study was supported by grants from the Bachmann-Strauss Dystonia & Parkinson Foundation, Inc., the Bendheim Parkinson's Disease Center, the Morris and Alma Schapiro Fund, and the NIH/NINDS (1 RO1 NS045999–01).

Publication of this supplement was supported by an educational grant from Teva Neuroscience and Eisai, Inc.

Disclosure: The sponsor has provided KM with an honorarium for his participation in this project and personal honoraria during his professional career. The sponsor has provided CWO with personal honoraria (in excess of $10,000) during his professional career. TJ, RJ, and AK have not reported any conflicts of interest.




This article has been cited by other articles:


Home page
Hum Mol GenetHome page
W. Yang, L. Chen, Y. Ding, X. Zhuang, and U. J. Kang
Paraquat induces dopaminergic dysfunction and proteasome impairment in DJ-1-deficient mice
Hum. Mol. Genet., December 1, 2007; 16(23): 2900 - 2910.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by AAN Enterprises, Inc.