Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.
Identifieur interne : 000735 ( PubMed/Checkpoint ); précédent : 000734; suivant : 000736Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.
Auteurs : Erwan Bezard [France] ; Zhenyu Yue ; Deniz Kirik ; Maria Grazia SpillantiniSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
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.
DOI: 10.1002/mds.25108
PubMed: 22753348
Affiliations:
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pubmed:22753348Le document en format XML
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<front><div type="abstract" xml:lang="en">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.</div>
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<MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName>
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<MeshHeading><DescriptorName UI="D051844" MajorTopicYN="N">alpha-Synuclein</DescriptorName>
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