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Abstract
Annual Review of Neuroscience
Vol. 28: 57-87 (Volume publication date July 2005)
(doi:10.1146/annurev.neuro.28.061604.135718)
First published online as a Review in Advance on January 25, 2005
MOLECULAR PATHOPHYSIOLOGY OF PARKINSON'S DISEASE

Darren J. Moore,1,2 Andrew B. West,1,2 Valina L. Dawson,1,2,3,4 and Ted M. Dawson1,2,3
1Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205; email:
2Departments of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205; email:
3Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205; email:
4Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205; email:

Parkinson's disease (PD) is a progressive neurodegenerative movement disorder that results primarily from the death of dopaminergic neurons in the substantia nigra. Although the etiology of PD is incompletely understood, the recent discovery of genes associated with rare monogenic forms of the disease, together with earlier studies and new experimental animal models, has provided important and novel insight into the molecular pathways involved in disease pathogenesis. Increasing evidence indicates that deficits in mitochondrial function, oxidative and nitrosative stress, the accumulation of aberrant or misfolded proteins, and ubiquitin-proteasome system dysfunction may represent the principal molecular pathways or events that commonly underlie the pathogenesis of sporadic and familial forms of PD .

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Authors:
Darren J. Moore
Andrew B. West
Valina L. Dawson
Ted M. Dawson
Keywords:
α-synuclein
parkin
mitochondrial complex-I
ubiquitin-proteasome system
oxidative stress

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