Pathogenesis of Parkinson's disease.
Identifieur interne : 000853 ( Main/Exploration ); précédent : 000852; suivant : 000854Pathogenesis of Parkinson's disease.
Auteurs : Etienne C. Hirsch [France] ; Peter Jenner ; Serge PrzedborskiSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
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.
DOI: 10.1002/mds.25032
PubMed: 22927094
Affiliations:
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Le document en format XML
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<country xml:lang="fr">France</country>
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<term>Nerve Degeneration (pathology)</term>
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<term>Neurons (pathology)</term>
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<front><div type="abstract" xml:lang="en">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.</div>
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