A tale of two factors: what determines the rate of progression in Huntington's disease? A longitudinal MRI study.
Identifieur interne : 001496 ( PubMed/Checkpoint ); précédent : 001495; suivant : 001497A 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 ; Gheorghe Doros ; Stephanie Y. Lee ; Tyler Triggs ; Keith Malarick ; Bruce Fischl ; David H. Salat ; Steven M. HerschSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- 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.
DOI: 10.1002/mds.23762
PubMed: 21611979
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"><nlm:affiliation>Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts, USA. rosas@helix.mgh.harvard.edu</nlm:affiliation><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></author><author><name sortKey="Reuter, Martin" sort="Reuter, Martin" uniqKey="Reuter M" first="Martin" last="Reuter">Martin Reuter</name></author><author><name sortKey="Doros, Gheorghe" sort="Doros, Gheorghe" uniqKey="Doros G" first="Gheorghe" last="Doros">Gheorghe Doros</name></author><author><name sortKey="Lee, Stephanie Y" sort="Lee, Stephanie Y" uniqKey="Lee S" first="Stephanie Y" last="Lee">Stephanie Y. 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Lee</name></author><author><name sortKey="Triggs, Tyler" sort="Triggs, Tyler" uniqKey="Triggs T" first="Tyler" last="Triggs">Tyler Triggs</name></author><author><name sortKey="Malarick, Keith" sort="Malarick, Keith" uniqKey="Malarick K" first="Keith" last="Malarick">Keith Malarick</name></author><author><name sortKey="Fischl, Bruce" sort="Fischl, Bruce" uniqKey="Fischl B" first="Bruce" last="Fischl">Bruce Fischl</name></author><author><name sortKey="Salat, David H" sort="Salat, David H" uniqKey="Salat D" first="David H" last="Salat">David H. Salat</name></author><author><name sortKey="Hersch, Steven M" sort="Hersch, Steven M" uniqKey="Hersch S" first="Steven M" last="Hersch">Steven M. Hersch</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age of Onset</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>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Trinucleotide Repeats (genetics)</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></textClass></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.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">21611979</PMID><DateCreated><Year>2011</Year><Month>08</Month><Day>10</Day></DateCreated><DateCompleted><Year>2011</Year><Month>12</Month><Day>08</Day></DateCompleted><DateRevised><Year>2014</Year><Month>10</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>9</Issue><PubDate><Year>2011</Year><Month>Aug</Month><Day>1</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>A tale of two factors: what determines the rate of progression in Huntington's disease? A longitudinal MRI study.</ArticleTitle><Pagination><MedlinePgn>1691-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23762</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>Copyright © 2011 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rosas</LastName><ForeName>H Diana</ForeName><Initials>HD</Initials><AffiliationInfo><Affiliation>Department of Neurology, Massachusetts General Hospital, Charlestown, Massachusetts, USA. rosas@helix.mgh.harvard.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Reuter</LastName><ForeName>Martin</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Doros</LastName><ForeName>Gheorghe</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Stephanie Y</ForeName><Initials>SY</Initials></Author><Author ValidYN="Y"><LastName>Triggs</LastName><ForeName>Tyler</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Malarick</LastName><ForeName>Keith</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Fischl</LastName><ForeName>Bruce</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Salat</LastName><ForeName>David H</ForeName><Initials>DH</Initials></Author><Author ValidYN="Y"><LastName>Hersch</LastName><ForeName>Steven M</ForeName><Initials>SM</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AG022381</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NR010827</GrantID><Acronym>NR</Acronym><Agency>NINR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS052585</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS05792</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS058793</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 NS058793-01A1</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41 RR014075</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41 RR014075-01A1</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41-RR14075</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 EB006758</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 EB006758-01A1</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NR010827</GrantID><Acronym>NR</Acronym><Agency>NINR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NR010827-01A1</GrantID><Acronym>NR</Acronym><Agency>NINR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS042861</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS042861</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS042861-01A2</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS052585</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS052585-01A1</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01EB006758</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS072652</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS072652-01</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21NS072652</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>RR021382</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U24 RR021382</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U24 RR021382-01</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U24-01</GrantID><Agency>PHS HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>05</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2000 Jan 25;54(2):452-8</RefSource><PMID Version="1">10668713</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>IEEE Trans Med Imaging. 2001 Jan;20(1):70-80</RefSource><PMID 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RefType="Cites"><RefSource>Neuroimage. 2010 Feb 15;49(4):2995-3004</RefSource><PMID Version="1">19850138</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2010 Apr;133(Pt 4):1094-110</RefSource><PMID Version="1">20375136</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroimage. 2010 Dec;53(4):1181-96</RefSource><PMID Version="1">20637289</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017668">Age of Onset</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001284">Atrophy</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002540">Cerebral Cortex</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018450">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006816">Huntington Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008137">Longitudinal Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D008279">Magnetic Resonance Imaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018911">Trinucleotide Repeats</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS284574</OtherID><OtherID Source="NLM">PMC3155608</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>10</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2011</Year><Month>2</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>3</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2011</Year><Month>5</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>5</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>5</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>12</Month><Day>13</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.23762</ArticleId><ArticleId IdType="pubmed">21611979</ArticleId><ArticleId IdType="pmc">PMC3155608</ArticleId><ArticleId IdType="mid">NIHMS284574</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region></list><tree><noCountry><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="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="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="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></noCountry><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></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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