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dc.contributor.authorVan Camp, Nadja-
dc.contributor.authorCamón, LLuïsa-
dc.contributor.authorVera, Núria de-
dc.contributor.authorMartínez, Emili-
dc.contributor.authorSoria, Guadalupe-
dc.contributor.authorSijbers, Jan-
dc.contributor.authorPlanas, Anna M.-
dc.contributor.authorLinden, Annemie van der-
dc.date.accessioned2013-04-02T09:43:26Z-
dc.date.available2013-04-02T09:43:26Z-
dc.date.issued2012-05-
dc.identifierdoi: 10.1016/j.neurobiolaging.2010.07.001-
dc.identifierissn: 0197-4580-
dc.identifier.citationNeurobiology of Aging 33(5): 945-959 (2012)-
dc.identifier.urihttp://hdl.handle.net/10261/73360-
dc.description.abstractIn vivo diffusion tensor imaging (DTI) was performed on the quinolinic acid (QUIN) rat model of Huntington's disease, together with behavioral assessment of motor deficits and histopathological characterization. DTI and histology revealed the presence of a cortical lesion in 53% of the QUIN animals (QUIN +ctx). Histologically, QUIN +ctx were distinguished from QUIN -ctx animals by increased astroglial reaction within a subregion of the caudate putamen and loss of white matter in the external capsula. Although both techniques are complementary, the quantitative character of DTI makes it possible to pick up subtle differences in tissue microstructure that are not identified with histology. DTI demonstrated differential changes of fractional anisotropy (FA), axial diffusivity (AD), radial diffusivity (RD), and mean diffusivity (MD) in the internal and external capsula, and within a subregion of the caudate putamen. It was suggested that FA increased due to a selective loss of the subcortical connections targeted by degenerative processes at the early stage of the disease, which might turn the striatum into a seemingly more organized structure. When tissue degeneration becomes more severe, FA decreased while AD, RD and MD increased. © 2012 Elsevier Inc.-
dc.description.sponsorshipThis study was funded in part by the EC FP6-project DiMI, LSHB-CT-2005-512146 to AP and AVDL; this study was supported by the Institute for the Promotion of Innovation by Science and Technology in Flanders (IWT SBO/030238 by the European Community (RATstream™ STREP, LSHM-CT-2007-037846) and Inter University At-traction Poles (IUAP-NIMI-P6/38) to AVDL. IB is holder of an IWT PhD grant, NVC is holder of an FWO Post-Doc grant.-
dc.language.isoeng-
dc.publisherElsevier-
dc.rightsclosedAccess-
dc.titleA complementary diffusion tensor imaging (DTI)-histological study in a model of Huntington's disease-
dc.typeartículo-
dc.identifier.doi10.1016/j.neurobiolaging.2010.07.001-
dc.relation.publisherversionhttp://dx.doi.org/10.1016/j.neurobiolaging.2010.07.001-
dc.date.updated2013-04-02T09:43:26Z-
dc.description.versionPeer Reviewed-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.openairetypeartículo-
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