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Parkinson's disease, proteins, and prions: milestones.

Identifieur interne : 001175 ( PubMed/Checkpoint ); précédent : 001174; suivant : 001176

Parkinson's disease, proteins, and prions: milestones.

Auteurs : C Warren Olanow [États-Unis] ; K. Mcnaught

Source :

Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.

RBID : pubmed:21626551

English descriptors

KwdEn :
- Animals, Autophagy (physiology), History, 20th Century, History, 21st Century, Humans, Lewy Bodies (pathology), Mutation (genetics), Nerve Tissue Proteins (genetics), Nerve Tissue Proteins (metabolism), Parkinson Disease (genetics), Parkinson Disease (history), Parkinson Disease (metabolism), Parkinson Disease (therapy), Prion Diseases (complications), Prion Diseases (genetics), Prion Diseases (metabolism), Prions (genetics), Prions (metabolism), Ubiquitin (metabolism).
MESH :
- chemical , genetics : Nerve Tissue Proteins, Prions.
- complications : Prion Diseases.
- genetics : Mutation, Parkinson Disease, Prion Diseases.
- history : Parkinson Disease.
- chemical , metabolism : Nerve Tissue Proteins, Parkinson Disease, Prion Diseases, Prions, Ubiquitin.
- pathology : Lewy Bodies.
- physiology : Autophagy.
- therapy : Parkinson Disease.
- Animals, History, 20th Century, History, 21st Century, Humans.

Abstract

Parkinson's disease (PD) is characterized by protein accumulation in the form of Lewy bodies and neurites. It is thus reasonable to consider that alterations in protein handling in the form of increased production, impaired clearance, or both might be central to the etiopathogenesis of the disease. Increasing genetic, laboratory and pathologic evidence has accumulated over the past 25 years supporting this hypothesis. A vicious cycle could develop in which increased protein accumulation from any cause could lead to interference with lysosomal and proteasomal clearance mechanisms causing further protein accumulation. Eventually, protein accumulation could overwhelm the cell's defenses and lead to the formation of toxic oligomers and amyloid-based inclusions such as Lewy bodies, disruption of critical cell processes, and ultimately neurodegeneration. More recent findings of Lewy pathology in implanted embryonic dopamine neurons in PD patients raises the intriguing possibility that PD might be a prion disorder. These concepts suggests new targets and novel candidate therapies that might be neuroprotective for PD.

DOI: 10.1002/mds.23767
PubMed: 21626551

Affiliations:

États-Unis

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Le document en format XML

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<author><name sortKey="Olanow, C Warren" sort="Olanow, C Warren" uniqKey="Olanow C" first="C Warren" last="Olanow">C Warren Olanow</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, New York 10029</wicri:regionArea>
<wicri:noRegion>New York 10029</wicri:noRegion>
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<term>Humans</term>
<term>Lewy Bodies (pathology)</term>
<term>Mutation (genetics)</term>
<term>Nerve Tissue Proteins (genetics)</term>
<term>Nerve Tissue Proteins (metabolism)</term>
<term>Parkinson Disease (genetics)</term>
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<term>Prion Diseases (genetics)</term>
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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is characterized by protein accumulation in the form of Lewy bodies and neurites. It is thus reasonable to consider that alterations in protein handling in the form of increased production, impaired clearance, or both might be central to the etiopathogenesis of the disease. Increasing genetic, laboratory and pathologic evidence has accumulated over the past 25 years supporting this hypothesis. A vicious cycle could develop in which increased protein accumulation from any cause could lead to interference with lysosomal and proteasomal clearance mechanisms causing further protein accumulation. Eventually, protein accumulation could overwhelm the cell's defenses and lead to the formation of toxic oligomers and amyloid-based inclusions such as Lewy bodies, disruption of critical cell processes, and ultimately neurodegeneration. More recent findings of Lewy pathology in implanted embryonic dopamine neurons in PD patients raises the intriguing possibility that PD might be a prion disorder. These concepts suggests new targets and novel candidate therapies that might be neuroprotective for PD.</div>
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<CopyrightInformation>Copyright © 2011 Movement Disorder Society.</CopyrightInformation>
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	Movement Disorders (revue)
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Movement Disorders (revue)

Parkinson's disease, proteins, and prions: milestones.

Parkinson's disease, proteins, and prions: milestones.

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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Pour générer des pages wiki