MovDisordV3, PascalFrancis, Corpus, bibRecord, 000574

Parkinson's Disease, Proteins, and Prions: Milestones

Identifieur interne : 000574 ( PascalFrancis/Corpus ); précédent : 000573; suivant : 000575

Parkinson's Disease, Proteins, and Prions: Milestones

Auteurs : C. Warren Olanow ; K. Mcnaught

Source :

Movement disorders [ 0885-3185 ] ; 2011.

RBID : Pascal:11-0264654

Descripteurs français

Pascal (Inist)
- Maladie de Parkinson, Pathologie du système nerveux, Protéine PrP, Prion.

English descriptors

KwdEn :
- Nervous system diseases, Parkinson disease, Prion, Prion protein.

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A08	`01`	`1`	`ENG`	`@1 Parkinson's Disease, Proteins, and Prions: Milestones`
A11	`01`	`1`		`@1 OLANOW (C. Warren)`
A11	`02`	`1`		`@1 MCNAUGHT (K.)`
A14	`01`			`@1 Department of Neurology and Neuroscience, Mount Sinai School of Medicine @2 New York, New York @3 USA @Z 1 aut.`
A14	`02`			`@1 National Tourette Syndrome Association @2 Bayside, New York @3 USA @Z 2 aut.`
A20				`@1 1056-1071`
A21				`@1 2011`
A23	`01`			`@0 ENG`
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A44				`@0 0000 @1 © 2011 INIST-CNRS. All rights reserved.`
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A47	`01`	`1`		`@0 11-0264654`
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A61				`@0 A`
A64	`01`	`1`		`@0 Movement disorders`
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C01	`01`		`ENG`	@0 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.
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C03	`02`	`X`	`FRE`	`@0 Pathologie du système nerveux @5 02`
C03	`02`	`X`	`ENG`	`@0 Nervous system diseases @5 02`
C03	`02`	`X`	`SPA`	`@0 Sistema nervioso patología @5 02`
C03	`03`	`X`	`FRE`	`@0 Protéine PrP @5 09`
C03	`03`	`X`	`ENG`	`@0 Prion protein @5 09`
C03	`03`	`X`	`SPA`	`@0 Protéina PrP @5 09`
C03	`04`	`X`	`FRE`	`@0 Prion @5 10`
C03	`04`	`X`	`ENG`	`@0 Prion @5 10`
C03	`04`	`X`	`SPA`	`@0 Prion @5 10`
C07	`01`	`X`	`FRE`	`@0 Pathologie de l'encéphale @5 37`
C07	`01`	`X`	`ENG`	`@0 Cerebral disorder @5 37`
C07	`01`	`X`	`SPA`	`@0 Encéfalo patología @5 37`
C07	`02`	`X`	`FRE`	`@0 Syndrome extrapyramidal @5 38`
C07	`02`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 38`
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C07	`03`	`X`	`FRE`	`@0 Maladie dégénérative @5 39`
C07	`03`	`X`	`ENG`	`@0 Degenerative disease @5 39`
C07	`03`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 39`
C07	`04`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 40`
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Format Inist (serveur)

NO :	PASCAL 11-0264654 INIST
ET :	Parkinson's Disease, Proteins, and Prions: Milestones
AU :	OLANOW (C. Warren); MCNAUGHT (K.)
AF :	Department of Neurology and Neuroscience, Mount Sinai School of Medicine/New York, New York/Etats-Unis (1 aut.); National Tourette Syndrome Association/Bayside, New York/Etats-Unis (2 aut.)
DT :	Publication en série; Niveau analytique
SO :	Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2011; Vol. 26; No. 6; Pp. 1056-1071; Bibl. 187 ref.
LA :	Anglais
EA :	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.
CC :	002B17; 002B17G
FD :	Maladie de Parkinson; Pathologie du système nerveux; Protéine PrP; Prion
FG :	Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central
ED :	Parkinson disease; Nervous system diseases; Prion protein; Prion
EG :	Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease
SD :	Parkinson enfermedad; Sistema nervioso patología; Protéina PrP; Prion
LO :	INIST-20953.354000191622890130
ID :	11-0264654

Links to Exploration step

Pascal:11-0264654

Le document en format XML

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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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	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 :

Descripteurs français

English descriptors

Abstract

Notice en format standard (ISO 2709)

Format Inist (serveur)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri