Pathogenesis of Parkinson's disease
Identifieur interne : 000E45 ( Main/Exploration ); précédent : 000E44; suivant : 000E46Pathogenesis of Parkinson's disease
Auteurs : Etienne C. Hirsch [France] ; Peter Jenner [Royaume-Uni] ; Serge Przedborski [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2013-01.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Calcium.
- complications : Mitochondrial Diseases.
- etiology : Parkinson Disease.
- metabolism : Neurons.
- pathology : Nerve Degeneration, Neurons, Parkinson Disease.
- physiology : Cell Death.
- Humans.
Abstract
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
Url:
DOI: 10.1002/mds.25032
Affiliations:
- France, Royaume-Uni, États-Unis
- Angleterre, Grand Londres, État de New York, Île-de-France
- Londres, Paris
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Le document en format XML
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<front><div type="abstract">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</div>
</front>
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