pubmed-article:20887870 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20887870 | lifeskim:mentions | umls-concept:C0030567 | lld:lifeskim |
pubmed-article:20887870 | lifeskim:mentions | umls-concept:C0003826 | lld:lifeskim |
pubmed-article:20887870 | lifeskim:mentions | umls-concept:C0026339 | lld:lifeskim |
pubmed-article:20887870 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
pubmed-article:20887870 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:20887870 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
pubmed-article:20887870 | lifeskim:mentions | umls-concept:C1442792 | lld:lifeskim |
pubmed-article:20887870 | lifeskim:mentions | umls-concept:C0314603 | lld:lifeskim |
pubmed-article:20887870 | pubmed:dateCreated | 2010-10-4 | lld:pubmed |
pubmed-article:20887870 | pubmed:abstractText | The identification of several mutations causing familial forms of Parkinson's disease (PD) has led to the creation of multiple lines of mice expressing similar genetic alterations. These models present a unique opportunity for understanding pathophysiological mechanisms leading to PD in a mammalian brain and provide models that are suitable for the preclinical testing of new therapies. Different lines of mice recapitulate the symptoms and pathological features of PD to various extents. This chapter examines their respective advantages and highlights some of the key findings that have already emerged from the analysis of these new models of PD. | lld:pubmed |
pubmed-article:20887870 | pubmed:language | eng | lld:pubmed |
pubmed-article:20887870 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20887870 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:20887870 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:20887870 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20887870 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20887870 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20887870 | pubmed:issn | 1875-7855 | lld:pubmed |
pubmed-article:20887870 | pubmed:author | pubmed-author:ChesseletMari... | lld:pubmed |
pubmed-article:20887870 | pubmed:author | pubmed-author:MagenIddoI | lld:pubmed |
pubmed-article:20887870 | pubmed:copyrightInfo | Copyright © 2010 Elsevier B.V. All rights reserved. | lld:pubmed |
pubmed-article:20887870 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20887870 | pubmed:volume | 184 | lld:pubmed |
pubmed-article:20887870 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20887870 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20887870 | pubmed:pagination | 53-87 | lld:pubmed |
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pubmed-article:20887870 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20887870 | pubmed:articleTitle | Genetic mouse models of Parkinson's disease The state of the art. | lld:pubmed |
pubmed-article:20887870 | pubmed:affiliation | Department of Neurology, David Geffen School of Medicine, UCLA, Los Angeles, CA, USA. | lld:pubmed |
pubmed-article:20887870 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20887870 | pubmed:publicationType | Review | lld:pubmed |