Pathogenesis of Parkinson's disease

Parkinson's disease is a common adult‐onset neurodegenerative disorder whose pathogenesis remains essentially unknown. Currently, it is believed that the neurodegenerative process in Parkinson's disease is a combination of both cell‐autonomous and non‐cell‐autonomous mechanisms. Proposed c...

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Bibliographic Details
Published in:	Movement disorders Vol. 28; no. 1; pp. 24 - 30
Main Authors:	Hirsch, Etienne C., Jenner, Peter, Przedborski, Serge
Format:	Journal Article
Language:	English
Published:	United States Blackwell Publishing Ltd 01-01-2013 Wiley Subscription Services, Inc
Subjects:	Calcium - metabolism Cell Death - physiology Dopamine neuron Humans inflammation misfolded protein mitochndria Mitochondrial Diseases - complications Movement disorders Nerve Degeneration - pathology neurodegeneration Neurons - metabolism Neurons - pathology Parkinson Disease - etiology Parkinson Disease - pathology
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Summary:	Parkinson's disease is a common adult‐onset neurodegenerative disorder whose pathogenesis remains essentially unknown. Currently, it is believed that the neurodegenerative process in Parkinson's disease is a combination of both cell‐autonomous and non‐cell‐autonomous mechanisms. Proposed cell‐autonomous mechanisms include alterations in mitochondrial bioenergetics, dysregulation of calcium homeostasis, and impaired turnover of mitochondria. As for the proposed non‐cell‐autonomous mechanisms, they involve prion‐like behavior of misfolded proteins and neuroinflammation. This suggests that cell death in Parkinson's disease is caused by a multifactorial cascade of pathogenic events and argues that effective neuroprotective therapy for Parkinson's disease may have to rely on multiple drug interventions. © 2013 Movement Disorder Society
Bibliography:	ark:/67375/WNG-6G7F0M0Z-3 ArticleID:MDS25032 istex:169622838E7D6D3DB3B55A5455A3D2869BCB4F91 Relevant conflicts of interest/financial disclosures Full financial disclosures and author roles may be found in the online version of this article. The authors are supported by grants from the National Institutes of Health (NS042269, NS064191, NS38370, NS070276, and NS072182 to S.P.), the U.S. Department of Defense (W81XWH‐08‐1‐0522, W81XWH‐08‐1‐0465, and W81XWH‐09‐1‐0245 to S.P.), the Parkinson Disease Foundation, the Thomas Hartman Foundation For Parkinson's Research, Project A.L.S, the Wings‐over‐Wall Street/Muscular Dystrophy Association. INSERM, CNRS, Université Pierre et Marie Curie, Cure Parkinson Foundation, Rosetrees Trust, Parkinson UK, and National Parkinson Foundation, Centre national de la recherche scientifique, Institut national de la santé et de la recherche médicale. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-2
ISSN:	0885-3185 1531-8257
DOI:	10.1002/mds.25032