MovDisordV3, PascalFrancis, Corpus, bibRecord, 000577

Milestones in Ataxia

Identifieur interne : 000577 ( PascalFrancis/Corpus ); précédent : 000576; suivant : 000578

Milestones in Ataxia

Auteurs : Thomas Klockgether ; Henry Paulson

Source :

Movement disorders [ 0885-3185 ] ; 2011.

RBID : Pascal:11-0264651

Descripteurs français

Pascal (Inist)
- Ataxie, Pathologie du système nerveux, Réparation, Ion, Trouble fonctionnel, Mitochondrie, Glutamine.

English descriptors

KwdEn :
- Ataxia, Dysfunction, Glutamine, Ions, Mitochondria, Nervous system diseases, Repair.

Abstract

The past 25 years have seen enormous progress in the deciphering of the genetic and molecular basis of ataxias, resulting in improved understanding of their pathogenesis. The most significant milestones during this period were the cloning of the genes associated with the common spinocerebellar ataxias, ataxia telangiectasia, and Friedreich ataxia. To date, the causative mutations of more than 30 spinocerebellar ataxias and 20 recessive ataxias have been identified. In addition, there are numerous acquired ataxias with defined molecular causes, so that the entire number of distinct ataxia disorders exceeds 50 and possibly approaches 100. Despite this enormous heterogeneity, a few recurrent pathophysiological themes stand out. These include protein aggregation, failure of protein homeostasis, perturbations in ion channel function, defects in DNA repair, and mitochondrial dysfunction. The clinical phenotypes of the most common ataxia disorders have been firmly established, and their natural history is being studied in ongoing large observational trials. Effective therapies for ataxias are still lacking. However, novel drug targets are under investigation, and it is expected that there will be an increasing number of therapeutic trials in ataxia.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A03		`1`		`@0 Mov. disord.`
A05				`@2 26`
A06				`@2 6`
A08	`01`	`1`	`ENG`	`@1 Milestones in Ataxia`
A11	`01`	`1`		`@1 KLOCKGETHER (Thomas)`
A11	`02`	`1`		`@1 PAULSON (Henry)`
A14	`01`			`@1 Department of Neurology, University Hospital Bonn @2 Bonn @3 DEU @Z 1 aut.`
A14	`02`			`@1 German Center for Neurodegenerative Disorder (DZNE) @2 Bonn @3 DEU @Z 1 aut.`
A14	`03`			`@1 Department of Neurology, University of Michigan @2 Ann Arbor, Michigan @3 USA @Z 2 aut.`
A20				`@1 1134-1141`
A21				`@1 2011`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 20953 @5 354000191622890190`
A44				`@0 0000 @1 © 2011 INIST-CNRS. All rights reserved.`
A45				`@0 48 ref.`
A47	`01`	`1`		`@0 11-0264651`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Movement disorders`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 The past 25 years have seen enormous progress in the deciphering of the genetic and molecular basis of ataxias, resulting in improved understanding of their pathogenesis. The most significant milestones during this period were the cloning of the genes associated with the common spinocerebellar ataxias, ataxia telangiectasia, and Friedreich ataxia. To date, the causative mutations of more than 30 spinocerebellar ataxias and 20 recessive ataxias have been identified. In addition, there are numerous acquired ataxias with defined molecular causes, so that the entire number of distinct ataxia disorders exceeds 50 and possibly approaches 100. Despite this enormous heterogeneity, a few recurrent pathophysiological themes stand out. These include protein aggregation, failure of protein homeostasis, perturbations in ion channel function, defects in DNA repair, and mitochondrial dysfunction. The clinical phenotypes of the most common ataxia disorders have been firmly established, and their natural history is being studied in ongoing large observational trials. Effective therapies for ataxias are still lacking. However, novel drug targets are under investigation, and it is expected that there will be an increasing number of therapeutic trials in ataxia.
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C02	`02`	`X`		`@0 002B17G`
C03	`01`	`X`	`FRE`	`@0 Ataxie @5 01`
C03	`01`	`X`	`ENG`	`@0 Ataxia @5 01`
C03	`01`	`X`	`SPA`	`@0 Ataxia @5 01`
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 Réparation @5 09`
C03	`03`	`X`	`ENG`	`@0 Repair @5 09`
C03	`03`	`X`	`SPA`	`@0 Reparación @5 09`
C03	`04`	`X`	`FRE`	`@0 Ion @2 NA @5 10`
C03	`04`	`X`	`ENG`	`@0 Ions @2 NA @5 10`
C03	`04`	`X`	`SPA`	`@0 Ión @2 NA @5 10`
C03	`05`	`X`	`FRE`	`@0 Trouble fonctionnel @5 11`
C03	`05`	`X`	`ENG`	`@0 Dysfunction @5 11`
C03	`05`	`X`	`SPA`	`@0 Trastorno funcional @5 11`
C03	`06`	`X`	`FRE`	`@0 Mitochondrie @5 12`
C03	`06`	`X`	`ENG`	`@0 Mitochondria @5 12`
C03	`06`	`X`	`SPA`	`@0 Mitocondria @5 12`
C03	`07`	`X`	`FRE`	`@0 Glutamine @2 NK @2 FR @5 13`
C03	`07`	`X`	`ENG`	`@0 Glutamine @2 NK @2 FR @5 13`
C03	`07`	`X`	`SPA`	`@0 Glutamina @2 NK @2 FR @5 13`
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 Pathologie du système nerveux central @5 38`
C07	`02`	`X`	`ENG`	`@0 Central nervous system disease @5 38`
C07	`02`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 38`
C07	`03`	`X`	`FRE`	`@0 Trouble neurologique @5 40`
C07	`03`	`X`	`ENG`	`@0 Neurological disorder @5 40`
C07	`03`	`X`	`SPA`	`@0 Trastorno neurológico @5 40`
N21				`@1 178`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 11-0264651 INIST
ET :	Milestones in Ataxia
AU :	KLOCKGETHER (Thomas); PAULSON (Henry)
AF :	Department of Neurology, University Hospital Bonn/Bonn/Allemagne (1 aut.); German Center for Neurodegenerative Disorder (DZNE)/Bonn/Allemagne (1 aut.); Department of Neurology, University of Michigan/Ann Arbor, Michigan/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. 1134-1141; Bibl. 48 ref.
LA :	Anglais
EA :	The past 25 years have seen enormous progress in the deciphering of the genetic and molecular basis of ataxias, resulting in improved understanding of their pathogenesis. The most significant milestones during this period were the cloning of the genes associated with the common spinocerebellar ataxias, ataxia telangiectasia, and Friedreich ataxia. To date, the causative mutations of more than 30 spinocerebellar ataxias and 20 recessive ataxias have been identified. In addition, there are numerous acquired ataxias with defined molecular causes, so that the entire number of distinct ataxia disorders exceeds 50 and possibly approaches 100. Despite this enormous heterogeneity, a few recurrent pathophysiological themes stand out. These include protein aggregation, failure of protein homeostasis, perturbations in ion channel function, defects in DNA repair, and mitochondrial dysfunction. The clinical phenotypes of the most common ataxia disorders have been firmly established, and their natural history is being studied in ongoing large observational trials. Effective therapies for ataxias are still lacking. However, novel drug targets are under investigation, and it is expected that there will be an increasing number of therapeutic trials in ataxia.
CC :	002B17; 002B17G
FD :	Ataxie; Pathologie du système nerveux; Réparation; Ion; Trouble fonctionnel; Mitochondrie; Glutamine
FG :	Pathologie de l'encéphale; Pathologie du système nerveux central; Trouble neurologique
ED :	Ataxia; Nervous system diseases; Repair; Ions; Dysfunction; Mitochondria; Glutamine
EG :	Cerebral disorder; Central nervous system disease; Neurological disorder
SD :	Ataxia; Sistema nervioso patología; Reparación; Ión; Trastorno funcional; Mitocondria; Glutamina
LO :	INIST-20953.354000191622890190
ID :	11-0264651

Links to Exploration step

Pascal:11-0264651

Le document en format XML

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<front><div type="abstract" xml:lang="en">The past 25 years have seen enormous progress in the deciphering of the genetic and molecular basis of ataxias, resulting in improved understanding of their pathogenesis. The most significant milestones during this period were the cloning of the genes associated with the common spinocerebellar ataxias, ataxia telangiectasia, and Friedreich ataxia. To date, the causative mutations of more than 30 spinocerebellar ataxias and 20 recessive ataxias have been identified. In addition, there are numerous acquired ataxias with defined molecular causes, so that the entire number of distinct ataxia disorders exceeds 50 and possibly approaches 100. Despite this enormous heterogeneity, a few recurrent pathophysiological themes stand out. These include protein aggregation, failure of protein homeostasis, perturbations in ion channel function, defects in DNA repair, and mitochondrial dysfunction. The clinical phenotypes of the most common ataxia disorders have been firmly established, and their natural history is being studied in ongoing large observational trials. Effective therapies for ataxias are still lacking. However, novel drug targets are under investigation, and it is expected that there will be an increasing number of therapeutic trials in ataxia.</div>
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<ET>Milestones in Ataxia</ET>
<AU>KLOCKGETHER (Thomas); PAULSON (Henry)</AU>
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<EA>The past 25 years have seen enormous progress in the deciphering of the genetic and molecular basis of ataxias, resulting in improved understanding of their pathogenesis. The most significant milestones during this period were the cloning of the genes associated with the common spinocerebellar ataxias, ataxia telangiectasia, and Friedreich ataxia. To date, the causative mutations of more than 30 spinocerebellar ataxias and 20 recessive ataxias have been identified. In addition, there are numerous acquired ataxias with defined molecular causes, so that the entire number of distinct ataxia disorders exceeds 50 and possibly approaches 100. Despite this enormous heterogeneity, a few recurrent pathophysiological themes stand out. These include protein aggregation, failure of protein homeostasis, perturbations in ion channel function, defects in DNA repair, and mitochondrial dysfunction. The clinical phenotypes of the most common ataxia disorders have been firmly established, and their natural history is being studied in ongoing large observational trials. Effective therapies for ataxias are still lacking. However, novel drug targets are under investigation, and it is expected that there will be an increasing number of therapeutic trials in ataxia.</EA>
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   |texte=   Milestones in Ataxia
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	Movement Disorders (revue)
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Movement Disorders (revue)

Milestones in Ataxia

Milestones in Ataxia

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