Movement Disorders (revue)

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Animal Models of Parkinson’s Disease: limits and relevance to neuroprotection studies

Identifieur interne : 000E87 ( Main/Exploration ); précédent : 000E86; suivant : 000E88

Animal Models of Parkinson’s Disease: limits and relevance to neuroprotection studies

Auteurs : Erwan Bezard [France] ; Zhenyu Yue [États-Unis] ; Deniz Kirik [Suède] ; Maria Grazia Spillantini [Royaume-Uni]

Source :

RBID : PMC:3517687

English descriptors

Abstract

Summary

Over the last two decades significant strides has been made towards acquiring a better knowledge of both the aetiology and pathogenesis of Parkinson’s disease (PD). Experimental models are of paramount importance to obtain greater insights into the pathogenesis of the disease. Thus far, neurotoxin-based animal models have been the most popular tools employed to produce selective neuronal death in both in vitro and in vivo systems. These models have been commonly referred to as the pathogenic models. The current trend in modelling PD revolves around what can be called the disease gene-based models, or etiologic models. The value of utilizing multiple models with different mechanism of insult rests on the premise that dopamine (DA) producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to down-regulation and overexpression of disease-related genes. In this position paper, we present the relevance of both pathogenic and etiologic models as well as the concept of clinically relevant designs that we argue should be utilized in the pre-clinical development phase of new neuroprotective therapies before embarking into clinical trials.


Url:
DOI: 10.1002/mds.25108
PubMed: 22753348
PubMed Central: 3517687


Affiliations:


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


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<p id="P2">Over the last two decades significant strides has been made towards acquiring a better knowledge of both the aetiology and pathogenesis of Parkinson’s disease (PD). Experimental models are of paramount importance to obtain greater insights into the pathogenesis of the disease. Thus far, neurotoxin-based animal models have been the most popular tools employed to produce selective neuronal death in both
<italic>in vitro</italic>
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<italic>in vivo</italic>
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<italic>pathogenic</italic>
models. The current trend in modelling PD revolves around what can be called the
<italic>disease gene-based</italic>
models, or
<italic>etiologic</italic>
models. The value of utilizing multiple models with different mechanism of insult rests on the premise that dopamine (DA) producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to down-regulation and overexpression of disease-related genes. In this position paper, we present the relevance of both pathogenic and etiologic models as well as the concept of clinically relevant designs that we argue should be utilized in the pre-clinical development phase of new neuroprotective therapies before embarking into clinical trials.</p>
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