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G03 Corpus callosal atrophy in Huntington's disease

Identifieur interne : 005537 ( Main/Exploration ); précédent : 005536; suivant : 005538

G03 Corpus callosal atrophy in Huntington's disease

Auteurs : He Crawford [Royaume-Uni] ; Nz Hobbs [Royaume-Uni] ; J. Cole [Royaume-Uni] ; Em Rees [Royaume-Uni] ; G. Owen [Royaume-Uni] ; Dr Langbehn [États-Unis] ; C. Frost [Royaume-Uni] ; B. Landwehrmeyer [Allemagne] ; R. Reilmann [Allemagne] ; D. Craufurd [Royaume-Uni] ; Jc Stout [Australie] ; A. Durr [France] ; B. Leavitt [Canada] ; Ra Roos [Pays-Bas] ; Sj Tabrizi [Royaume-Uni] ; Ri Scahill [Royaume-Uni]

Source :

RBID : ISTEX:F5CA874DE78DE98E65D05D4283D1B3CC98696C71

Descripteurs français

English descriptors

Abstract

Background Research into Huntington's disease (HD) has revealed white-matter loss in individuals more than 10 years prior to predicted disease onset, focused around the striatum, corpus callosum (CC) and posterior white-matter tracts. Degeneration of the CC is of interest since it provides interhemispheric connections to cortical areas known to be affected in HD. Aims This study aims to investigate the utility of volumetric measurements of the CC in HD using a novel segmentation technique, multiple time-points and a large well-characterised cohort. Structure-function relationship in the CC will also be explored. Methods Volumetric 3T MRI from controls, premanifest gene carriers and early HD subjects enrolled in the TRACK-HD study will be analysed at baseline and 24 months. The CC will be delineated using a semi-automated segmentation protocol. Differences in baseline volumes and atrophy rates between groups will be examined, as well as correlations between volume loss and clinical impairment. Results Preliminary analysis of a subset of subjects indicates that early HD subjects have reduced CC volume compared with controls and premanifest subjects (p<0.001). Increased longitudinal CC volume change was found in early HD subjects, compared with controls (p<0.001). Interestingly there was significant difference in longitudinal change between controls and premanifest subjects close to disease onset (p<0.05). This work will be extended to include multi-site data and correlations between atrophy and clinical and cognitive decline. Conclusions Measurement of CC atrophy may have potential as an imaging biomarker for HD and may prove useful for exploring interhemispheric structure-function relationships. Funding Helen Crawford is supported by the CHDI Foundation, a not for profit organisation dedicated to finding treatments for HD.

Url:
DOI: 10.1136/jnnp-2012-303524.83


Affiliations:


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Le document en format XML

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<term>White matter volume</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr">
<term>Neurologie</term>
<term>Santé publique</term>
</keywords>
</textClass>
<langUsage>
<language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front>
<div type="abstract">Background Research into Huntington's disease (HD) has revealed white-matter loss in individuals more than 10 years prior to predicted disease onset, focused around the striatum, corpus callosum (CC) and posterior white-matter tracts. Degeneration of the CC is of interest since it provides interhemispheric connections to cortical areas known to be affected in HD. Aims This study aims to investigate the utility of volumetric measurements of the CC in HD using a novel segmentation technique, multiple time-points and a large well-characterised cohort. Structure-function relationship in the CC will also be explored. Methods Volumetric 3T MRI from controls, premanifest gene carriers and early HD subjects enrolled in the TRACK-HD study will be analysed at baseline and 24 months. The CC will be delineated using a semi-automated segmentation protocol. Differences in baseline volumes and atrophy rates between groups will be examined, as well as correlations between volume loss and clinical impairment. Results Preliminary analysis of a subset of subjects indicates that early HD subjects have reduced CC volume compared with controls and premanifest subjects (p<0.001). Increased longitudinal CC volume change was found in early HD subjects, compared with controls (p<0.001). Interestingly there was significant difference in longitudinal change between controls and premanifest subjects close to disease onset (p<0.05). This work will be extended to include multi-site data and correlations between atrophy and clinical and cognitive decline. Conclusions Measurement of CC atrophy may have potential as an imaging biomarker for HD and may prove useful for exploring interhemispheric structure-function relationships. Funding Helen Crawford is supported by the CHDI Foundation, a not for profit organisation dedicated to finding treatments for HD.</div>
</front>
</TEI>
<affiliations>
<list>
<country>
<li>Allemagne</li>
<li>Australie</li>
<li>Canada</li>
<li>France</li>
<li>Pays-Bas</li>
<li>Royaume-Uni</li>
<li>États-Unis</li>
</country>
<region>
<li>Angleterre</li>
<li>Bade-Wurtemberg</li>
<li>District de Münster</li>
<li>District de Tübingen</li>
<li>Grand Londres</li>
<li>Grand Manchester</li>
<li>Hollande-Méridionale</li>
<li>Iowa</li>
<li>Rhénanie-du-Nord-Westphalie</li>
<li>Île-de-France</li>
</region>
<settlement>
<li>Iowa City</li>
<li>Leyde</li>
<li>Londres</li>
<li>Manchester</li>
<li>Münster</li>
<li>Paris</li>
<li>Ulm</li>
</settlement>
<orgName>
<li>University College de Londres</li>
<li>Université de Manchester</li>
<li>Université de l'Iowa</li>
</orgName>
</list>
<tree>
<country name="Royaume-Uni">
<region name="Angleterre">
<name sortKey="Crawford, He" sort="Crawford, He" uniqKey="Crawford H" first="He" last="Crawford">He Crawford</name>
</region>
<name sortKey="Cole, J" sort="Cole, J" uniqKey="Cole J" first="J" last="Cole">J. Cole</name>
<name sortKey="Craufurd, D" sort="Craufurd, D" uniqKey="Craufurd D" first="D" last="Craufurd">D. Craufurd</name>
<name sortKey="Frost, C" sort="Frost, C" uniqKey="Frost C" first="C" last="Frost">C. Frost</name>
<name sortKey="Hobbs, Nz" sort="Hobbs, Nz" uniqKey="Hobbs N" first="Nz" last="Hobbs">Nz Hobbs</name>
<name sortKey="Owen, G" sort="Owen, G" uniqKey="Owen G" first="G" last="Owen">G. Owen</name>
<name sortKey="Rees, Em" sort="Rees, Em" uniqKey="Rees E" first="Em" last="Rees">Em Rees</name>
<name sortKey="Scahill, Ri" sort="Scahill, Ri" uniqKey="Scahill R" first="Ri" last="Scahill">Ri Scahill</name>
<name sortKey="Tabrizi, Sj" sort="Tabrizi, Sj" uniqKey="Tabrizi S" first="Sj" last="Tabrizi">Sj Tabrizi</name>
</country>
<country name="États-Unis">
<region name="Iowa">
<name sortKey="Langbehn, Dr" sort="Langbehn, Dr" uniqKey="Langbehn D" first="Dr" last="Langbehn">Dr Langbehn</name>
</region>
<name sortKey="Langbehn, Dr" sort="Langbehn, Dr" uniqKey="Langbehn D" first="Dr" last="Langbehn">Dr Langbehn</name>
</country>
<country name="Allemagne">
<region name="Bade-Wurtemberg">
<name sortKey="Landwehrmeyer, B" sort="Landwehrmeyer, B" uniqKey="Landwehrmeyer B" first="B" last="Landwehrmeyer">B. Landwehrmeyer</name>
</region>
<name sortKey="Reilmann, R" sort="Reilmann, R" uniqKey="Reilmann R" first="R" last="Reilmann">R. Reilmann</name>
</country>
<country name="Australie">
<noRegion>
<name sortKey="Stout, Jc" sort="Stout, Jc" uniqKey="Stout J" first="Jc" last="Stout">Jc Stout</name>
</noRegion>
</country>
<country name="France">
<region name="Île-de-France">
<name sortKey="Durr, A" sort="Durr, A" uniqKey="Durr A" first="A" last="Durr">A. Durr</name>
</region>
</country>
<country name="Canada">
<noRegion>
<name sortKey="Leavitt, B" sort="Leavitt, B" uniqKey="Leavitt B" first="B" last="Leavitt">B. Leavitt</name>
</noRegion>
</country>
<country name="Pays-Bas">
<region name="Hollande-Méridionale">
<name sortKey="Roos, Ra" sort="Roos, Ra" uniqKey="Roos R" first="Ra" last="Roos">Ra Roos</name>
</region>
</country>
</tree>
</affiliations>
</record>

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