MovDisordV3, PubMed, Checkpoint, bibRecord, 001244

Milestones in ataxia.

Identifieur interne : 001244 ( PubMed/Checkpoint ); précédent : 001243; suivant : 001245

Milestones in ataxia.

Auteurs : Thomas Klockgether [Allemagne] ; Henry Paulson

Source :

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

RBID : pubmed:21626557

English descriptors

KwdEn :
- Animals, Ataxia (classification), Ataxia (genetics), Ataxia (history), Ataxia (therapy), Biomedical Research (history), Biomedical Research (methods), History, 20th Century, History, 21st Century, Humans.
MESH :
- classification : Ataxia.
- genetics : Ataxia.
- history : Ataxia, Biomedical Research.
- methods : Biomedical Research.
- therapy : Ataxia.
- Animals, History, 20th Century, History, 21st Century, Humans.

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.

DOI: 10.1002/mds.23559
PubMed: 21626557

Affiliations:

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

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Links to Exploration step

pubmed:21626557

Le document en format XML

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<affiliation wicri:level="3"><nlm:affiliation>Department of Neurology, University Hospital Bonn, Bonn, Germany. klockgether@uni-bonn.de</nlm:affiliation>
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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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	Movement Disorders (revue)
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Movement Disorders (revue)

Milestones in ataxia.

Milestones in ataxia.

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)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki