Animal models of Parkinson's disease: Limits and relevance to neuroprotection studies
Identifieur interne : 000F10 ( Main/Exploration ); précédent : 000F09; suivant : 000F11Animal 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 :
- Movement Disorders [ 0885-3185 ] ; 2013-01.
English descriptors
- KwdEn :
- Animals, Disease Models, Animal, Genetic Vectors (adverse effects), Humans, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Mice, Mice, Transgenic, Mutation (genetics), Neuroprotective Agents (therapeutic use), Neurotoxins (toxicity), Parkinson Disease (drug therapy), Parkinson Disease (etiology), Protein-Serine-Threonine Kinases (genetics), alpha-Synuclein (genetics).
- MESH :
- chemical , genetics : Protein-Serine-Threonine Kinases, alpha-Synuclein.
- chemical , therapeutic use : Neuroprotective Agents.
- chemical , toxicity : Neurotoxins.
- chemical : Leucine-Rich Repeat Serine-Threonine Protein Kinase-2.
- adverse effects : Genetic Vectors.
- drug therapy : Parkinson Disease.
- etiology : Parkinson Disease.
- genetics : Mutation.
- Animals, Disease Models, Animal, Humans, Mice, Mice, Transgenic.
Abstract
Over the last two decades, significant strides has been made toward acquiring a better knowledge of both the etiology 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 modeling PD revolves around what can be called the disease gene‐based models or etiologic models. The value of utilizing multiple models with a different mechanism of insult rests on the premise that dopamine‐producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to downregulation and overexpression of disease‐related genes. In this position article, 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 preclinical development phase of new neuroprotective therapies before embarking into clinical trials. © 2013 Movement Disorder Society
Url:
- https://api.istex.fr/document/9F298F088399FE2F79399EFC5EDDAB3F6976D4F4/fulltext/pdf
- https://hal.archives-ouvertes.fr/hal-01290064
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3517687
DOI: 10.1002/mds.25108
Affiliations:
- France, Royaume-Uni, Suède, États-Unis
- Angleterre, Angleterre de l'Est, Aquitaine, Nouvelle-Aquitaine, État de New York
- Bordeaux, Cambridge
- Université de Cambridge
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Le document en format XML
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Transgenic</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Over the last two decades, significant strides has been made toward acquiring a better knowledge of both the etiology 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 modeling PD revolves around what can be called the disease gene‐based models or etiologic models. The value of utilizing multiple models with a different mechanism of insult rests on the premise that dopamine‐producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to downregulation and overexpression of disease‐related genes. In this position article, 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 preclinical development phase of new neuroprotective therapies before embarking into clinical trials. © 2013 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>France</li><li>Royaume-Uni</li><li>Suède</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Angleterre de l'Est</li><li>Aquitaine</li><li>Nouvelle-Aquitaine</li><li>État de New York</li></region><settlement><li>Bordeaux</li><li>Cambridge</li></settlement><orgName><li>Université de Cambridge</li></orgName></list><tree><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name></region><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name></country><country name="États-Unis"><region name="État de New York"><name sortKey="Yue, Zhenyu" sort="Yue, Zhenyu" uniqKey="Yue Z" first="Zhenyu" last="Yue">Zhenyu Yue</name></region></country><country name="Suède"><noRegion><name sortKey="Kirik, Deniz" sort="Kirik, Deniz" uniqKey="Kirik D" first="Deniz" last="Kirik">Deniz Kirik</name></noRegion></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Spillantini, Maria Grazia" sort="Spillantini, Maria Grazia" uniqKey="Spillantini M" first="Maria Grazia" last="Spillantini">Maria Grazia Spillantini</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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