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MOLECULAR PATHOPHYSIOLOGY OF PARKINSON'S DISEASE

Annual Review of Neuroscience · 2005 · Vol. 28(1) · pp. 57–87
Darren J. MooreAndrew B. WestValina L. DawsonTed M. Dawson

Abstract

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 .

Parkinson's Disease Mechanisms and TreatmentsNeurological diseases and metabolismCellular transport and secretionSubstantia nigraParkinson's diseasePathogenesisNeuroscienceDopaminergicDiseaseBiologyOxidative stressParkinPathophysiology

MeSH terms

Protein Deglycase DJ-1PTEN-Induced Putative KinaseAnimalsHumansModels, BiologicalMutationNerve Tissue ProteinsParkinson DiseaseProtein KinasesSignal TransductionOncogene ProteinsUbiquitinUbiquitin ThiolesteraseUbiquitin-Protein LigasesProteasome Endopeptidase Complex
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References
Parkinson's Disease
Neuron · 2003 · 5,394 citations
α-Synuclein Promotes Mitochondrial Deficit and Oxidative Stress
American Journal Of Pathology · 2000 · 708 citations
Oxidative stress in Parkinson's disease
Annals of Neurology · 2003 · 2,042 citations
Mitochondrial Complex I Deficiency in Parkinson's Disease
Journal of Neurochemistry · 1990 · 2,261 citations
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