Source:http://linkedlifedata.com/resource/pubmed/id/19150499
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2009-3-23
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| pubmed:abstractText |
Members of the GDNF family of ligands, including neurturin (NTN), have been implicated as potential therapeutic agents for Huntington's disease (HD). The present study examined the ability of CERE-120 (AAV2-NTN) to provide structural and functional protection in the N171-82Q transgenic HD mouse model. AAV2-NTN therapy attenuated rotorod deficits in this mutant relative to control treated transgenics (p<0.01). AAV2-NTN treatment significantly reduced the number of transgenic mice that exhibited clasping behavior and partially restored their stride lengths (both p<0.05). Stereological counts of NeuN-ir neurons revealed a significant neuroprotection in the striatum of AAV2-NTN treated relative to control treated transgenics (p<0.001). Most fascinating, stereological counts of NeuN-labeled cells in layers V-VI of prefrontal cortex revealed that intrastriatal AAV2-NTN administration prevented the loss of frontal cortical NeuN-ir neurons seen in transgenic mice (p<0.01). These data indicate that gene delivery of NTN may be a viable strategy for the treatment of this incurable disease.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Huntington protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/NeuN protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Neurturin,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
1095-953X
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
34
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
40-50
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| pubmed:meshHeading |
pubmed-meshheading:19150499-Animals,
pubmed-meshheading:19150499-Cerebral Cortex,
pubmed-meshheading:19150499-Corpus Striatum,
pubmed-meshheading:19150499-Dependovirus,
pubmed-meshheading:19150499-Disease Models, Animal,
pubmed-meshheading:19150499-Gene Expression,
pubmed-meshheading:19150499-Gene Therapy,
pubmed-meshheading:19150499-Gene Transfer Techniques,
pubmed-meshheading:19150499-Genetic Vectors,
pubmed-meshheading:19150499-Huntington Disease,
pubmed-meshheading:19150499-Mice,
pubmed-meshheading:19150499-Mice, Transgenic,
pubmed-meshheading:19150499-Motor Activity,
pubmed-meshheading:19150499-Mutation,
pubmed-meshheading:19150499-Nerve Tissue Proteins,
pubmed-meshheading:19150499-Neurons,
pubmed-meshheading:19150499-Neurturin,
pubmed-meshheading:19150499-Nuclear Proteins,
pubmed-meshheading:19150499-Random Allocation,
pubmed-meshheading:19150499-Rotarod Performance Test
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| pubmed:year |
2009
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| pubmed:articleTitle |
Intrastriatal CERE-120 (AAV-Neurturin) protects striatal and cortical neurons and delays motor deficits in a transgenic mouse model of Huntington's disease.
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| pubmed:affiliation |
Department of Neurological Sciences, Rush University Medical Center, 1735 West Harrison Street, Suite 300, Chicago, IL 60612, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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