Animal Models of Parkinson’s Disease: A Gateway to Therapeutics?
Identifieur interne : 000087 ( Pmc/Checkpoint ); précédent : 000086; suivant : 000088Animal Models of Parkinson’s Disease: A Gateway to Therapeutics?
Auteurs : Weidong Le [République populaire de Chine] ; Pavani Sayana ; Joseph Jankovic [États-Unis]Source :
- Neurotherapeutics [ 1933-7213 ] ; 2013.
Abstract
Parkinson’s disease (PD) is a progressive, neurodegenerative disorder of unknown etiology, although a complex interaction between environmental and genetic factors has been implicated as a pathogenic mechanism of selected neuronal loss. A better understanding of the etiology, pathogenesis, and molecular mechanisms underlying the disease process may be gained from research on animal models. While cell and tissue models are helpful in unraveling involved molecular pathways, animal models are much better suited to study the pathogenesis and potential treatment strategies. The animal models most relevant to PD include those generated by neurotoxic chemicals that selectively disrupt the catecholaminergic system such as 6-hydroxydopamine; 1-methyl-1,2,3,6-tetrahydropiridine; agricultural pesticide toxins, such as rotenone and paraquat; the ubiquitin proteasome system inhibitors; inflammatory modulators; and several genetically manipulated models, such as α-synuclein, DJ-1, PINK1, Parkin, and leucine-rich repeat kinase 2 transgenic or knock-out animals. Genetic and nongenetic animal models have their own unique advantages and limitations, which must be considered when they are employed in the study of pathogenesis or treatment approaches. This review provides a summary and a critical review of our current knowledge about various
The online version of this article (doi:10.1007/s13311-013-0234-1) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1007/s13311-013-0234-1
PubMed: 24158912
PubMed Central: 3899493
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Parkinson’s disease (PD) is a progressive, neurodegenerative disorder of unknown etiology, although a complex interaction between environmental and genetic factors has been implicated as a pathogenic mechanism of selected neuronal loss. A better understanding of the etiology, pathogenesis, and molecular mechanisms underlying the disease process may be gained from research on animal models. While cell and tissue models are helpful in unraveling involved molecular pathways, animal models are much better suited to study the pathogenesis and potential treatment strategies. The animal models most relevant to PD include those generated by neurotoxic chemicals that selectively disrupt the catecholaminergic system such as 6-hydroxydopamine; 1-methyl-1,2,3,6-tetrahydropiridine; agricultural pesticide toxins, such as rotenone and paraquat; the ubiquitin proteasome system inhibitors; inflammatory modulators; and several genetically manipulated models, such as α-synuclein, DJ-1, PINK1, Parkin, and leucine-rich repeat kinase 2 transgenic or knock-out animals. Genetic and nongenetic animal models have their own unique advantages and limitations, which must be considered when they are employed in the study of pathogenesis or treatment approaches. This review provides a summary and a critical review of our current knowledge about various <italic>in vivo</italic>
models of PD used to test novel therapeutic strategies.</p>
<sec><title>Electronic supplementary material</title>
<p>The online version of this article (doi:10.1007/s13311-013-0234-1) contains supplementary material, which is available to authorized users.</p>
</sec>
</div>
</front>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Neurotherapeutics</journal-id>
<journal-id journal-id-type="iso-abbrev">Neurotherapeutics</journal-id>
<journal-title-group><journal-title>Neurotherapeutics</journal-title>
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<issn pub-type="ppub">1933-7213</issn>
<issn pub-type="epub">1878-7479</issn>
<publisher><publisher-name>Springer US</publisher-name>
<publisher-loc>Boston</publisher-loc>
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<article-id pub-id-type="doi">10.1007/s13311-013-0234-1</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
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<title-group><article-title>Animal Models of Parkinson’s Disease: A Gateway to Therapeutics?</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Le</surname>
<given-names>Weidong</given-names>
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<address><email>wdle@sibs.ac.cn</email>
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<contrib contrib-type="author"><name><surname>Sayana</surname>
<given-names>Pavani</given-names>
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<contrib contrib-type="author" corresp="yes"><name><surname>Jankovic</surname>
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<aff id="Aff1"><label></label>
1st Affiliated Hospital, Dalian Medical University, Dalian, 116011 China</aff>
<aff id="Aff2"><label></label>
Department of Medicine, Gandhi Medical College, Padmarao Nagar, Secunderabad, AP 500020 India</aff>
<aff id="Aff3"><label></label>
Parkinson’s Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX 77030 USA</aff>
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<pub-date pub-type="epub"><day>25</day>
<month>10</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="ppub"><month>1</month>
<year>2014</year>
</pub-date>
<volume>11</volume>
<issue>1</issue>
<fpage>92</fpage>
<lpage>110</lpage>
<permissions><copyright-statement>© The American Society for Experimental NeuroTherapeutics, Inc. 2013</copyright-statement>
</permissions>
<abstract id="Abs1"><p>Parkinson’s disease (PD) is a progressive, neurodegenerative disorder of unknown etiology, although a complex interaction between environmental and genetic factors has been implicated as a pathogenic mechanism of selected neuronal loss. A better understanding of the etiology, pathogenesis, and molecular mechanisms underlying the disease process may be gained from research on animal models. While cell and tissue models are helpful in unraveling involved molecular pathways, animal models are much better suited to study the pathogenesis and potential treatment strategies. The animal models most relevant to PD include those generated by neurotoxic chemicals that selectively disrupt the catecholaminergic system such as 6-hydroxydopamine; 1-methyl-1,2,3,6-tetrahydropiridine; agricultural pesticide toxins, such as rotenone and paraquat; the ubiquitin proteasome system inhibitors; inflammatory modulators; and several genetically manipulated models, such as α-synuclein, DJ-1, PINK1, Parkin, and leucine-rich repeat kinase 2 transgenic or knock-out animals. Genetic and nongenetic animal models have their own unique advantages and limitations, which must be considered when they are employed in the study of pathogenesis or treatment approaches. This review provides a summary and a critical review of our current knowledge about various <italic>in vivo</italic>
models of PD used to test novel therapeutic strategies.</p>
<sec><title>Electronic supplementary material</title>
<p>The online version of this article (doi:10.1007/s13311-013-0234-1) contains supplementary material, which is available to authorized users.</p>
</sec>
</abstract>
<kwd-group xml:lang="en"><title>Keywords</title>
<kwd>Parkinson’s disease</kwd>
<kwd>animal models</kwd>
<kwd>neurotoxins</kwd>
<kwd>transgenic</kwd>
<kwd>motor symptoms</kwd>
<kwd>non-motor symptoms</kwd>
<kwd>therapeutics</kwd>
<kwd>neuroprotection</kwd>
</kwd-group>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© The American Society for Experimental NeuroTherapeutics, Inc. 2014</meta-value>
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</front>
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