Rate and Acceleration of Whole-Brain Atrophy in Premanifest and Early Huntington's Disease
Identifieur interne : 002201 ( PascalFrancis/Curation ); précédent : 002200; suivant : 002202Rate and Acceleration of Whole-Brain Atrophy in Premanifest and Early Huntington's Disease
Auteurs : Edward J. Wild [Royaume-Uni] ; Susie M. D. Henley [Royaume-Uni] ; Nicola Z. Hobbs [Royaume-Uni] ; Chris Frost [Royaume-Uni] ; David G. Macmanus [Royaume-Uni] ; Roger A. Barker [Royaume-Uni] ; Nick C. Fox [Royaume-Uni] ; Sarah J. Tabrizi [Royaume-Uni]Source :
- Movement disorders [ 0885-3185 ] ; 2010.
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- Pascal (Inist)
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Abstract
Huntington's disease (HD) produces progressive and ultimately widespread impairment ot bram function. Neostriatal atrophy alone cannot account for whole-brain losses seen postmortem, and the mutant huntingtin protein and its neuropathologic sequelae are evident throughout the brain. Whole-brain atrophy quantification encompasses the totality of mutant huntingtin's effects on brain volume and may be useful in tracking progression in trials. We studied whole-brain atrophy in HD using a 2-year follow-up design, with three annual MRI scans. We recruited 20 control subjects, 21 premanifest mutation carriers, and 40 patients with early HD and used the brain boundary shift integral to study rate and acceleration of atrophy. Among subjects with an acceptable quality 2-year scan pair, age- and gender-standardized mean brain atrophy rate was greater (P < 0.001) in the patients with HD (n = 21; 0.88%/yr; 95% confidence interval: 0.62-1.13%/yr) than that in controls (n = 13; 0.16%/yr; 0.00-0.32%/yr). In the 12 patients with early HD in whom acceleration could be directly assessed there was evidence (P = 0.048) of acceleration year-on-year (mean acceleration = 0.69% yr-2; 95% confidence interval: 0.01 % yr-2 to 1.37% yr-2), although this was not formally significantly different from that in controls (n = 7, P = 0.055). Statistically significantly increased atrophy rates and acceleration were not seen overall in the premanifest group, who were on average 18 years from predicted disease onset. We conclude that the study of whole-brain atrophy has the potential to inform our understanding of the neurobiology of HD and warrants further study as one means of assessing the outcomes of future clinical trials.
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Rate and Acceleration of Whole-Brain Atrophy in Premanifest and Early Huntington's Disease</title><author><name sortKey="Wild, Edward J" sort="Wild, Edward J" uniqKey="Wild E" first="Edward J." last="Wild">Edward J. Wild</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Dementia Research Centre, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Neurodegenerative Disease, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Henley, Susie M D" sort="Henley, Susie M D" uniqKey="Henley S" first="Susie M. D." last="Henley">Susie M. D. 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Tabrizi</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Neurodegenerative Disease, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">10-0288336</idno><date when="2010">2010</date><idno type="stanalyst">PASCAL 10-0288336 INIST</idno><idno type="RBID">Pascal:10-0288336</idno><idno type="wicri:Area/PascalFrancis/Corpus">000B18</idno><idno type="wicri:Area/PascalFrancis/Curation">002201</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Rate and Acceleration of Whole-Brain Atrophy in Premanifest and Early Huntington's Disease</title><author><name sortKey="Wild, Edward J" sort="Wild, Edward J" uniqKey="Wild E" first="Edward J." last="Wild">Edward J. Wild</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Dementia Research Centre, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Neurodegenerative Disease, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Henley, Susie M D" sort="Henley, Susie M D" uniqKey="Henley S" first="Susie M. D." last="Henley">Susie M. D. Henley</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Dementia Research Centre, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Neurodegenerative Disease, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Hobbs, Nicola Z" sort="Hobbs, Nicola Z" uniqKey="Hobbs N" first="Nicola Z." last="Hobbs">Nicola Z. Hobbs</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Dementia Research Centre, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Neurodegenerative Disease, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Frost, Chris" sort="Frost, Chris" uniqKey="Frost C" first="Chris" last="Frost">Chris Frost</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Dementia Research Centre, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Medical Statistics Unit, London School of Hygiene and Tropical Medicine</s1><s2>London</s2><s3>GBR</s3><sZ>4 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Macmanus, David G" sort="Macmanus, David G" uniqKey="Macmanus D" first="David G." last="Macmanus">David G. Macmanus</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>NMR Research Unit, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Barker, Roger A" sort="Barker, Roger A" uniqKey="Barker R" first="Roger A." last="Barker">Roger A. Barker</name><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Department of Clinical Neurosciences, Brain Repair Centre, Addenbrooke's Hospital</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>6 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Fox, Nick C" sort="Fox, Nick C" uniqKey="Fox N" first="Nick C." last="Fox">Nick C. Fox</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Dementia Research Centre, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Neurodegenerative Disease, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Tabrizi, Sarah J" sort="Tabrizi, Sarah J" uniqKey="Tabrizi S" first="Sarah J." last="Tabrizi">Sarah J. Tabrizi</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Neurodegenerative Disease, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Atrophy</term><term>Encephalon</term><term>Huntington disease</term><term>Nervous system diseases</term><term>Nuclear magnetic resonance imaging</term><term>Volumetric analysis</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Atrophie</term><term>Chorée de Huntington</term><term>Pathologie du système nerveux</term><term>Encéphale</term><term>Volumétrie</term><term>Imagerie RMN</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Huntington's disease (HD) produces progressive and ultimately widespread impairment ot bram function. Neostriatal atrophy alone cannot account for whole-brain losses seen postmortem, and the mutant huntingtin protein and its neuropathologic sequelae are evident throughout the brain. Whole-brain atrophy quantification encompasses the totality of mutant huntingtin's effects on brain volume and may be useful in tracking progression in trials. We studied whole-brain atrophy in HD using a 2-year follow-up design, with three annual MRI scans. We recruited 20 control subjects, 21 premanifest mutation carriers, and 40 patients with early HD and used the brain boundary shift integral to study rate and acceleration of atrophy. Among subjects with an acceptable quality 2-year scan pair, age- and gender-standardized mean brain atrophy rate was greater (P < 0.001) in the patients with HD (n = 21; 0.88%/yr; 95% confidence interval: 0.62-1.13%/yr) than that in controls (n = 13; 0.16%/yr; 0.00-0.32%/yr). In the 12 patients with early HD in whom acceleration could be directly assessed there was evidence (P = 0.048) of acceleration year-on-year (mean acceleration = 0.69% yr<sup>-2</sup>; 95% confidence interval: 0.01 % yr<sup>-2</sup> to 1.37% yr<sup>-2</sup>), although this was not formally significantly different from that in controls (n = 7, P = 0.055). Statistically significantly increased atrophy rates and acceleration were not seen overall in the premanifest group, who were on average 18 years from predicted disease onset. We conclude that the study of whole-brain atrophy has the potential to inform our understanding of the neurobiology of HD and warrants further study as one means of assessing the outcomes of future clinical trials.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>25</s2></fA05><fA06><s2>7</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Rate and Acceleration of Whole-Brain Atrophy in Premanifest and Early Huntington's Disease</s1></fA08><fA11 i1="01" i2="1"><s1>WILD (Edward J.)</s1></fA11><fA11 i1="02" i2="1"><s1>HENLEY (Susie M. D.)</s1></fA11><fA11 i1="03" i2="1"><s1>HOBBS (Nicola Z.)</s1></fA11><fA11 i1="04" i2="1"><s1>FROST (Chris)</s1></fA11><fA11 i1="05" i2="1"><s1>MACMANUS (David G.)</s1></fA11><fA11 i1="06" i2="1"><s1>BARKER (Roger A.)</s1></fA11><fA11 i1="07" i2="1"><s1>FOX (Nick C.)</s1></fA11><fA11 i1="08" i2="1"><s1>TABRIZI (Sarah J.)</s1></fA11><fA14 i1="01"><s1>Dementia Research Centre, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Neurodegenerative Disease, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ></fA14><fA14 i1="03"><s1>Medical Statistics Unit, London School of Hygiene and Tropical Medicine</s1><s2>London</s2><s3>GBR</s3><sZ>4 aut.</sZ></fA14><fA14 i1="04"><s1>NMR Research Unit, UCL Institute of Neurology</s1><s2>London</s2><s3>GBR</s3><sZ>5 aut.</sZ></fA14><fA14 i1="05"><s1>Department of Clinical Neurosciences, Brain Repair Centre, Addenbrooke's Hospital</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>6 aut.</sZ></fA14><fA20><s1>888-895</s1></fA20><fA21><s1>2010</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000193040220110</s5></fA43><fA44><s0>0000</s0><s1>© 2010 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>31 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>10-0288336</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Movement disorders</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Huntington's disease (HD) produces progressive and ultimately widespread impairment ot bram function. Neostriatal atrophy alone cannot account for whole-brain losses seen postmortem, and the mutant huntingtin protein and its neuropathologic sequelae are evident throughout the brain. Whole-brain atrophy quantification encompasses the totality of mutant huntingtin's effects on brain volume and may be useful in tracking progression in trials. We studied whole-brain atrophy in HD using a 2-year follow-up design, with three annual MRI scans. We recruited 20 control subjects, 21 premanifest mutation carriers, and 40 patients with early HD and used the brain boundary shift integral to study rate and acceleration of atrophy. Among subjects with an acceptable quality 2-year scan pair, age- and gender-standardized mean brain atrophy rate was greater (P < 0.001) in the patients with HD (n = 21; 0.88%/yr; 95% confidence interval: 0.62-1.13%/yr) than that in controls (n = 13; 0.16%/yr; 0.00-0.32%/yr). In the 12 patients with early HD in whom acceleration could be directly assessed there was evidence (P = 0.048) of acceleration year-on-year (mean acceleration = 0.69% yr<sup>-2</sup>; 95% confidence interval: 0.01 % yr<sup>-2</sup> to 1.37% yr<sup>-2</sup>), although this was not formally significantly different from that in controls (n = 7, P = 0.055). Statistically significantly increased atrophy rates and acceleration were not seen overall in the premanifest group, who were on average 18 years from predicted disease onset. We conclude that the study of whole-brain atrophy has the potential to inform our understanding of the neurobiology of HD and warrants further study as one means of assessing the outcomes of future clinical trials.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17</s0></fC02><fC02 i1="02" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Atrophie</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Atrophy</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Atrofia</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Chorée de Huntington</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Huntington disease</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Corea Huntington</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Encéphale</s0><s5>09</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Encephalon</s0><s5>09</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Encéfalo</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Volumétrie</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Volumetric analysis</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Volumetría</s0><s5>10</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Imagerie RMN</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Nuclear magnetic resonance imaging</s0><s5>11</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Imaginería RMN</s0><s5>11</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Central nervous system</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie héréditaire</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Genetic disease</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0><s5>41</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>42</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>42</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>42</s5></fC07><fN21><s1>186</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard></inist></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Rate and Acceleration of Whole-Brain Atrophy in Premanifest and Early Huntington's Disease
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