ParkinsonFranceV1, Main, Exploration, bibRecord, 001437

ANIMAL MODELS OF MULTIPLE SYSTEM ATROPHY

Identifieur interne : 001437 ( Main/Exploration ); précédent : 001436; suivant : 001438

ANIMAL MODELS OF MULTIPLE SYSTEM ATROPHY

Auteurs : P.-O. Fernagut [France] ; F. Tison [France]

Source :

Neuroscience [ 0306-4522 ] ; 2012.

RBID : Pascal:12-0292457

Descripteurs français

Pascal (Inist)
- Modèle animal, Lévodopa, Noyau gris central, Oligodendrocyte, Atrophie multisystématisée, Maladie de Parkinson, Synucléine α.

English descriptors

KwdEn :
- Animal model, Basal ganglion, Levodopa, Multiple system atrophy, Oligodendrocyte, Parkinson disease, α-synuclein.

Abstract

Multiple system atrophy (MSA) is a sporadic adult-onset neurodegenerative disorder clinically characterized by a variable combination of dysautonomia, levodopa-unresponsive parkinsonian and cerebellar symptoms. Neurodegeneration in MSA occurs in the substantia nigra, putamen, inferior olive, pontine and brainstem nuclei, as well as intermediolateral cell column of the spinal cord. MSA is recognized as a synucleinopathy due to the accumulation of insoluble alpha-synuclein in oligodendroglial cytoplasmic inclusions. Several animal models have been developed in order to reproduce various clinical and pathological features of MSA. Using "double toxin-double lesion" or "single toxin- double lesion", neurotoxin-based models were designed in rats, mice and non-human primates to reproduce the neuropathology of MSA in the nigrostriatal system while gene-based models were developed in mice to reproduce the accumulation of insoluble alpha-synuclein in oligodendrocytes. Both approaches have then been merged to create optimized, dual-hit models. This review describes the different animal models of MSA, their respective advantages and limitations and their usefulness to decipher the pathophysiology of MSA then to define efficient symptomatic and disease-modifying therapies.

Affiliations:

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

to stream PascalFrancis, to step Corpus: 000234
to stream PascalFrancis, to step Curation: 001087
to stream PascalFrancis, to step Checkpoint: 000235
to stream Main, to step Merge: 001499
to stream Main, to step Curation: 001437

Le document en format XML

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<front><div type="abstract" xml:lang="en">Multiple system atrophy (MSA) is a sporadic adult-onset neurodegenerative disorder clinically characterized by a variable combination of dysautonomia, levodopa-unresponsive parkinsonian and cerebellar symptoms. Neurodegeneration in MSA occurs in the substantia nigra, putamen, inferior olive, pontine and brainstem nuclei, as well as intermediolateral cell column of the spinal cord. MSA is recognized as a synucleinopathy due to the accumulation of insoluble alpha-synuclein in oligodendroglial cytoplasmic inclusions. Several animal models have been developed in order to reproduce various clinical and pathological features of MSA. Using "double toxin-double lesion" or "single toxin- double lesion", neurotoxin-based models were designed in rats, mice and non-human primates to reproduce the neuropathology of MSA in the nigrostriatal system while gene-based models were developed in mice to reproduce the accumulation of insoluble alpha-synuclein in oligodendrocytes. Both approaches have then been merged to create optimized, dual-hit models. This review describes the different animal models of MSA, their respective advantages and limitations and their usefulness to decipher the pathophysiology of MSA then to define efficient symptomatic and disease-modifying therapies.</div>
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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

ANIMAL MODELS OF MULTIPLE SYSTEM ATROPHY

ANIMAL MODELS OF MULTIPLE SYSTEM ATROPHY

Source :

Descripteurs français

English descriptors

Abstract

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

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri