A tale of two factors: What determines the rate of progression in Huntington's disease? A longitudinal MRI study
Identifieur interne : 001831 ( Main/Exploration ); précédent : 001830; suivant : 001832A tale of two factors: What determines the rate of progression in Huntington's disease? A longitudinal MRI study
Auteurs : H. Diana Rosas [États-Unis] ; Martin Reuter [États-Unis] ; Gheorghe Doros [États-Unis] ; Stephanie Y. Lee [États-Unis] ; Tyler Triggs [États-Unis] ; Keith Malarick [États-Unis] ; Bruce Fischl [États-Unis] ; David H. Salat [États-Unis] ; Steven M. Hersch [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-08-01.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Age of Onset, Atrophy, Atrophy (pathology), Cerebral Cortex (pathology), Disease Progression, Female, Humans, Huntington Disease (genetics), Huntington Disease (pathology), Huntington Disease (physiopathology), Huntington disease, Huntington's disease, Longitudinal Studies, Magnetic Resonance Imaging, Male, Nervous system diseases, Nuclear magnetic resonance imaging, Trinucleotide Repeats (genetics), Variability, magnetic resonance imaging longitudinal atrophy, neurodegeneration, phenotypic variability.
- MESH :
- genetics : Huntington Disease, Trinucleotide Repeats.
- pathology : Atrophy, Cerebral Cortex, Huntington Disease.
- physiopathology : Huntington Disease.
- Age of Onset, Disease Progression, Female, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male.
Abstract
Over the past several years, increased attention has been devoted to understanding regionally selective brain changes that occur in Huntington's disease and their relationships to phenotypic variability. Clinical progression is also heterogeneous, and although CAG repeat length influences age of onset, its role, if any, in progression has been less clear. We evaluated progression in Huntington's disease using a novel longitudinal magnetic resonance imaging analysis. Our hypothesis was that the rate of brain atrophy is influenced by the age of onset of Huntington's disease. We scanned 22 patients with Huntington's disease at approximately 1‐year intervals; individuals were divided into 1 of 3 groups, determined by the relative age of onset. We found significant differences in the rates of atrophy of cortex, white matter, and subcortical structures; patients who developed symptoms earlier demonstrated the most rapid rates of atrophy compared with those who developed symptoms during middle age or more advanced age. Rates of cortical atrophy were topologically variable, with the most rapid changes occurring in sensorimotor, posterior frontal, and portions of the parietal cortex. There were no significant differences in the rates of atrophy in basal ganglia structures. Although both CAG repeat length and age influenced the rate of change in some regions, there was no significant correlation in many regions. Rates of regional brain atrophy seem to be influenced by the age of onset of Huntington's disease symptoms and are only partially explained by CAG repeat length. These findings suggest that other genetic, epigenetic, and environmental factors play important roles in neurodegeneration in Huntington's disease. © 2011 Movement Disorder Society
Url:
- https://api.istex.fr/document/1E7657C3F7DAF305FEE000BF8071B8700766B9A6/fulltext/pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3155608
DOI: 10.1002/mds.23762
Affiliations:
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A longitudinal MRI study</title><author><name sortKey="Rosas, H Diana" sort="Rosas, H Diana" uniqKey="Rosas H" first="H. Diana" last="Rosas">H. Diana Rosas</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Neuro‐imaging of Aging and Neurodegenerative Diseases, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>MassGeneral Institute for Neurodegeneration, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Reuter, Martin" sort="Reuter, Martin" uniqKey="Reuter M" first="Martin" last="Reuter">Martin Reuter</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Neuro‐imaging of Aging and Neurodegenerative Diseases, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Athinoula A. 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Lee</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Neuro‐imaging of Aging and Neurodegenerative Diseases, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>MassGeneral Institute for Neurodegeneration, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Triggs, Tyler" sort="Triggs, Tyler" uniqKey="Triggs T" first="Tyler" last="Triggs">Tyler Triggs</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Neuro‐imaging of Aging and Neurodegenerative Diseases, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>MassGeneral Institute for Neurodegeneration, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Malarick, Keith" sort="Malarick, Keith" uniqKey="Malarick K" first="Keith" last="Malarick">Keith Malarick</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Neuro‐imaging of Aging and Neurodegenerative Diseases, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>MassGeneral Institute for Neurodegeneration, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Fischl, Bruce" sort="Fischl, Bruce" uniqKey="Fischl B" first="Bruce" last="Fischl">Bruce Fischl</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Radiology, Massachusetts General Hospital, Charlestown, Massachusetts, USA, and Harvard Medical School, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>MIT Computer Science and AI Lab, Division of Health Sciences and Technology, Cambridge, Masschusetts</wicri:regionArea><wicri:noRegion>Masschusetts</wicri:noRegion></affiliation></author><author><name sortKey="Salat, David H" sort="Salat, David H" uniqKey="Salat D" first="David H." last="Salat">David H. Salat</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for Neuro‐imaging of Aging and Neurodegenerative Diseases, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Radiology, Massachusetts General Hospital, Charlestown, Massachusetts, USA, and Harvard Medical School, Boston, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Hersch, Steven M" sort="Hersch, Steven M" uniqKey="Hersch S" first="Steven M." last="Hersch">Steven M. Hersch</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>MassGeneral Institute for Neurodegeneration, Massachusetts General Hospital, Charlestown, Massachusetts</wicri:regionArea><placeName><region type="state">Massachusetts</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-08-01">2011-08-01</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1691">1691</biblScope><biblScope unit="page" to="1697">1697</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">1E7657C3F7DAF305FEE000BF8071B8700766B9A6</idno><idno type="DOI">10.1002/mds.23762</idno><idno type="ArticleID">MDS23762</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age of Onset</term><term>Atrophy</term><term>Atrophy (pathology)</term><term>Cerebral Cortex (pathology)</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Huntington Disease (genetics)</term><term>Huntington Disease (pathology)</term><term>Huntington Disease (physiopathology)</term><term>Huntington disease</term><term>Huntington's disease</term><term>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Nervous system diseases</term><term>Nuclear magnetic resonance imaging</term><term>Trinucleotide Repeats (genetics)</term><term>Variability</term><term>magnetic resonance imaging longitudinal atrophy</term><term>neurodegeneration</term><term>phenotypic variability</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Huntington Disease</term><term>Trinucleotide Repeats</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Atrophy</term><term>Cerebral Cortex</term><term>Huntington Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Huntington Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age of Onset</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Atrophie</term><term>Chorée de Huntington</term><term>Imagerie RMN</term><term>Pathologie du système nerveux</term><term>Variabilité</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Over the past several years, increased attention has been devoted to understanding regionally selective brain changes that occur in Huntington's disease and their relationships to phenotypic variability. Clinical progression is also heterogeneous, and although CAG repeat length influences age of onset, its role, if any, in progression has been less clear. We evaluated progression in Huntington's disease using a novel longitudinal magnetic resonance imaging analysis. Our hypothesis was that the rate of brain atrophy is influenced by the age of onset of Huntington's disease. We scanned 22 patients with Huntington's disease at approximately 1‐year intervals; individuals were divided into 1 of 3 groups, determined by the relative age of onset. We found significant differences in the rates of atrophy of cortex, white matter, and subcortical structures; patients who developed symptoms earlier demonstrated the most rapid rates of atrophy compared with those who developed symptoms during middle age or more advanced age. Rates of cortical atrophy were topologically variable, with the most rapid changes occurring in sensorimotor, posterior frontal, and portions of the parietal cortex. There were no significant differences in the rates of atrophy in basal ganglia structures. Although both CAG repeat length and age influenced the rate of change in some regions, there was no significant correlation in many regions. Rates of regional brain atrophy seem to be influenced by the age of onset of Huntington's disease symptoms and are only partially explained by CAG repeat length. These findings suggest that other genetic, epigenetic, and environmental factors play important roles in neurodegeneration in Huntington's disease. © 2011 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region></list><tree><country name="États-Unis"><region name="Massachusetts"><name sortKey="Rosas, H Diana" sort="Rosas, H Diana" uniqKey="Rosas H" first="H. Diana" last="Rosas">H. Diana Rosas</name></region><name sortKey="Doros, Gheorghe" sort="Doros, Gheorghe" uniqKey="Doros G" first="Gheorghe" last="Doros">Gheorghe Doros</name><name sortKey="Fischl, Bruce" sort="Fischl, Bruce" uniqKey="Fischl B" first="Bruce" last="Fischl">Bruce Fischl</name><name sortKey="Fischl, Bruce" sort="Fischl, Bruce" uniqKey="Fischl B" first="Bruce" last="Fischl">Bruce Fischl</name><name sortKey="Fischl, Bruce" sort="Fischl, Bruce" uniqKey="Fischl B" first="Bruce" last="Fischl">Bruce Fischl</name><name sortKey="Hersch, Steven M" sort="Hersch, Steven M" uniqKey="Hersch S" first="Steven M." last="Hersch">Steven M. Hersch</name><name sortKey="Hersch, Steven M" sort="Hersch, Steven M" uniqKey="Hersch S" first="Steven M." last="Hersch">Steven M. Hersch</name><name sortKey="Lee, Stephanie Y" sort="Lee, Stephanie Y" uniqKey="Lee S" first="Stephanie Y." last="Lee">Stephanie Y. Lee</name><name sortKey="Lee, Stephanie Y" sort="Lee, Stephanie Y" uniqKey="Lee S" first="Stephanie Y." last="Lee">Stephanie Y. Lee</name><name sortKey="Lee, Stephanie Y" sort="Lee, Stephanie Y" uniqKey="Lee S" first="Stephanie Y." last="Lee">Stephanie Y. Lee</name><name sortKey="Lee, Stephanie Y" sort="Lee, Stephanie Y" uniqKey="Lee S" first="Stephanie Y." last="Lee">Stephanie Y. Lee</name><name sortKey="Malarick, Keith" sort="Malarick, Keith" uniqKey="Malarick K" first="Keith" last="Malarick">Keith Malarick</name><name sortKey="Malarick, Keith" sort="Malarick, Keith" uniqKey="Malarick K" first="Keith" last="Malarick">Keith Malarick</name><name sortKey="Malarick, Keith" sort="Malarick, Keith" uniqKey="Malarick K" first="Keith" last="Malarick">Keith Malarick</name><name sortKey="Malarick, Keith" sort="Malarick, Keith" uniqKey="Malarick K" first="Keith" last="Malarick">Keith Malarick</name><name sortKey="Reuter, Martin" sort="Reuter, Martin" uniqKey="Reuter M" first="Martin" last="Reuter">Martin Reuter</name><name sortKey="Reuter, Martin" sort="Reuter, Martin" uniqKey="Reuter M" first="Martin" last="Reuter">Martin Reuter</name><name sortKey="Reuter, Martin" sort="Reuter, Martin" uniqKey="Reuter M" first="Martin" last="Reuter">Martin Reuter</name><name sortKey="Reuter, Martin" sort="Reuter, Martin" uniqKey="Reuter M" first="Martin" last="Reuter">Martin Reuter</name><name sortKey="Reuter, Martin" sort="Reuter, Martin" uniqKey="Reuter M" first="Martin" last="Reuter">Martin Reuter</name><name sortKey="Rosas, H Diana" sort="Rosas, H Diana" uniqKey="Rosas H" first="H. Diana" last="Rosas">H. Diana Rosas</name><name sortKey="Rosas, H Diana" sort="Rosas, H Diana" uniqKey="Rosas H" first="H. Diana" last="Rosas">H. Diana Rosas</name><name sortKey="Rosas, H Diana" sort="Rosas, H Diana" uniqKey="Rosas H" first="H. Diana" last="Rosas">H. Diana Rosas</name><name sortKey="Salat, David H" sort="Salat, David H" uniqKey="Salat D" first="David H." last="Salat">David H. Salat</name><name sortKey="Salat, David H" sort="Salat, David H" uniqKey="Salat D" first="David H." last="Salat">David H. Salat</name><name sortKey="Salat, David H" sort="Salat, David H" uniqKey="Salat D" first="David H." last="Salat">David H. Salat</name><name sortKey="Triggs, Tyler" sort="Triggs, Tyler" uniqKey="Triggs T" first="Tyler" last="Triggs">Tyler Triggs</name><name sortKey="Triggs, Tyler" sort="Triggs, Tyler" uniqKey="Triggs T" first="Tyler" last="Triggs">Tyler Triggs</name><name sortKey="Triggs, Tyler" sort="Triggs, Tyler" uniqKey="Triggs T" first="Tyler" last="Triggs">Tyler Triggs</name><name sortKey="Triggs, Tyler" sort="Triggs, Tyler" uniqKey="Triggs T" first="Tyler" last="Triggs">Tyler Triggs</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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