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Human Molecular Genetics Advance Access originally published online on August 26, 2005
Human Molecular Genetics 2005 14(18):2749-2755; doi:10.1093/hmg/ddi308
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© The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Molecular pathogenesis of Parkinson's disease

Sonia Gandhi and Nicholas W. Wood*

Department of Molecular Neuroscience, Institute of Neurology, Queen Square, London

* To whom correspondence should be addressed. Email: n.wood{at}ion.ucl.ac.uk

Received August 2, 2005; Accepted August 6, 2005

Parkinson's disease (PD) is a common and incurable neurodegenerative disease, affecting 1% of the population over the age of 65. Despite a well-described clinical and pathological phenotype, the molecular mechanisms which lead to neurodegeneration remain elusive. However, there is a wealth of evidence from both toxin based models and genetic based models, which suggest a major etiologic role for mitochondrial dysfunction, protein aggregation, the ubiquitin–proteasome system and kinase signalling pathways in the pathogenesis of PD. Ultimately, an understanding of the molecular events which precipitate neurodegeneration in idiopathic PD will enable the development of targeted and effective therapeutic strategies. We review the latest evidence for the proposed molecular processes and discuss their relevance to the pathogenesis of sporadic PD.


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