Brain Metabolite Alterations and Cognitive Dysfunction in Early Huntington's Disease
Identifieur interne : 000159 ( PascalFrancis/Corpus ); précédent : 000158; suivant : 000160Brain Metabolite Alterations and Cognitive Dysfunction in Early Huntington's Disease
Auteurs : Paul G. Unschuld ; Richard A. E. Edden ; Aaron Carass ; XINYANG LIU ; Megan Shanahan ; XIN WANG ; Kenichi Oishi ; Jason Brandt ; Susan S. Bassett ; Graham W. Redgrave ; Russell L. Margolis ; Peter C. M. Van Zijl ; Peter B. Barker ; Christopher A. RossSource :
- Movement disorders [ 0885-3185 ] ; 2012.
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English descriptors
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Abstract
Huntington's disease (HD) is a neurodegenerative disorder characterized by early cognitive decline that progresses at later stages to dementia and severe movement disorder. HD is caused by a cytosine-adenine- guanine triplet-repeat expansion mutation in the Huntingtin gene, allowing early diagnosis by genetic testing. This study aimed to identify the relationship of N-acetylaspartate and other brain metabolites to cognitive function in HD-mutation carriers by using high-field-strength magnetic resonance spectroscopy (MRS) at 7 Tesla. Twelve individuals with the HD mutation in premanifest or early-stage disease versus 12 healthy controls underwent 1H magnetic resonance spectroscopy (7.2 mL voxel in the posterior cingulate cortex) at 7 Tesla, and also T1-weighted structural magnetic resonance imaging. All participants received standardized tests of cognitive functioning including the Montreal Cognitive Assessment and standardized quantified neurological examination within an hour before scanning. Individuals with the HD mutation had significantly lower posterior cingulate cortex N-acetylaspartate (-9.6%, P =.02) and glutamate (-10.1 %, P = .02) levels than did controls. In contrast, in this small group, measures of brain morphology including striatal and ventricle volumes did not differ significantly. Linear regression with Montreal Cognitive Assessment scores revealed significant correlations with N-acetylaspartate (r2 = 0.50, P = .01) and glutamate (NAA) (r2 = 0.64, P = .002) in HD subjects. Our data suggest a relationship between reduced N-acetylaspartate and glutamate levels in the posterior cingulate cortex with cognitive decline in the early stages of HD. N-acetylaspartate and glutamate magnetic resonance spectroscopy signals of the posterior cingulate cortex region may serve as potential biomarkers of disease progression or treatment outcome in HD and other neurodegenerative disorders with early cognitive dysfunction, when structural brain changes are still minor.
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Format Inist (serveur)
| NO : | PASCAL 12-0280048 INIST |
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| ET : | Brain Metabolite Alterations and Cognitive Dysfunction in Early Huntington's Disease |
| AU : | UNSCHULD (Paul G.); EDDEN (Richard A. E.); CARASS (Aaron); XINYANG LIU; SHANAHAN (Megan); XIN WANG; OISHI (Kenichi); BRANDT (Jason); BASSETT (Susan S.); REDGRAVE (Graham W.); MARGOLIS (Russell L.); VAN ZIJL (Peter C. M.); BARKER (Peter B.); ROSS (Christopher A.) |
| AF : | Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine/Baltimore, Maryland/Etats-Unis (1 aut., 5 aut., 8 aut., 9 aut., 10 aut., 11 aut., 14 aut.); Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine/Baltimore, Maryland/Etats-Unis (2 aut., 3 aut., 6 aut., 7 aut., 12 aut., 13 aut.); F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute/Baltimore, Maryland/Etats-Unis (2 aut., 12 aut., 13 aut.); Brigham and Women's Hospital, Harvard Medical School/Boston, Massachusetts/Etats-Unis (4 aut.); Department of Neurology, Johns Hopkins University School of Medicine/Baltimore, Maryland/Etats-Unis (8 aut., 11 aut., 14 aut.); Department of Neuroscience and Pharmacology, Johns Hopkins University School of Medicine/Baltimore, Maryland/Etats-Unis (14 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2012; Vol. 27; No. 7; Pp. 895-902; Bibl. 65 ref. |
| LA : | Anglais |
| EA : | Huntington's disease (HD) is a neurodegenerative disorder characterized by early cognitive decline that progresses at later stages to dementia and severe movement disorder. HD is caused by a cytosine-adenine- guanine triplet-repeat expansion mutation in the Huntingtin gene, allowing early diagnosis by genetic testing. This study aimed to identify the relationship of N-acetylaspartate and other brain metabolites to cognitive function in HD-mutation carriers by using high-field-strength magnetic resonance spectroscopy (MRS) at 7 Tesla. Twelve individuals with the HD mutation in premanifest or early-stage disease versus 12 healthy controls underwent 1H magnetic resonance spectroscopy (7.2 mL voxel in the posterior cingulate cortex) at 7 Tesla, and also T1-weighted structural magnetic resonance imaging. All participants received standardized tests of cognitive functioning including the Montreal Cognitive Assessment and standardized quantified neurological examination within an hour before scanning. Individuals with the HD mutation had significantly lower posterior cingulate cortex N-acetylaspartate (-9.6%, P =.02) and glutamate (-10.1 %, P = .02) levels than did controls. In contrast, in this small group, measures of brain morphology including striatal and ventricle volumes did not differ significantly. Linear regression with Montreal Cognitive Assessment scores revealed significant correlations with N-acetylaspartate (r2 = 0.50, P = .01) and glutamate (NAA) (r2 = 0.64, P = .002) in HD subjects. Our data suggest a relationship between reduced N-acetylaspartate and glutamate levels in the posterior cingulate cortex with cognitive decline in the early stages of HD. N-acetylaspartate and glutamate magnetic resonance spectroscopy signals of the posterior cingulate cortex region may serve as potential biomarkers of disease progression or treatment outcome in HD and other neurodegenerative disorders with early cognitive dysfunction, when structural brain changes are still minor. |
| CC : | 002B17; 002B17G |
| FD : | Trouble cognitif; Chorée de Huntington; Dégénérescence; Pathologie du système nerveux; Encéphale; Métabolite; Glutamate; Cognition |
| FG : | Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Maladie héréditaire; Pathologie du système nerveux central; Aminoacide excitateur; Neurotransmetteur |
| ED : | Cognitive disorder; Huntington disease; Degeneration; Nervous system diseases; Encephalon; Metabolite; Glutamate; Cognition |
| EG : | Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Genetic disease; Central nervous system disease; Excitatory aminoacid; Neurotransmitter |
| SD : | Trastorno cognitivo; Corea Huntington; Degeneración; Sistema nervioso patología; Encéfalo; Metabolito; Glutamato; Cognición |
| LO : | INIST-20953.354000508307110130 |
| ID : | 12-0280048 |
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Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Barker, Peter B" sort="Barker, Peter B" uniqKey="Barker P" first="Peter B." last="Barker">Peter B. Barker</name><affiliation><inist:fA14 i1="02"><s1>Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ross, Christopher A" sort="Ross, Christopher A" uniqKey="Ross C" first="Christopher A." last="Ross">Christopher A. Ross</name><affiliation><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Department of Neurology, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>8 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="06"><s1>Department of Neuroscience and Pharmacology, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>14 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">12-0280048</idno><date when="2012">2012</date><idno type="stanalyst">PASCAL 12-0280048 INIST</idno><idno type="RBID">Pascal:12-0280048</idno><idno type="wicri:Area/PascalFrancis/Corpus">000159</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Brain Metabolite Alterations and Cognitive Dysfunction in Early Huntington's Disease</title><author><name sortKey="Unschuld, Paul G" sort="Unschuld, Paul G" uniqKey="Unschuld P" first="Paul G." last="Unschuld">Paul G. Unschuld</name><affiliation><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Edden, Richard A E" sort="Edden, Richard A E" uniqKey="Edden R" first="Richard A. E." last="Edden">Richard A. E. Edden</name><affiliation><inist:fA14 i1="02"><s1>Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Carass, Aaron" sort="Carass, Aaron" uniqKey="Carass A" first="Aaron" last="Carass">Aaron Carass</name><affiliation><inist:fA14 i1="02"><s1>Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Xinyang Liu" sort="Xinyang Liu" uniqKey="Xinyang Liu" last="Xinyang Liu">XINYANG LIU</name><affiliation><inist:fA14 i1="04"><s1>Brigham and Women's Hospital, Harvard Medical School</s1><s2>Boston, Massachusetts</s2><s3>USA</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Shanahan, Megan" sort="Shanahan, Megan" uniqKey="Shanahan M" first="Megan" last="Shanahan">Megan Shanahan</name><affiliation><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Xin Wang" sort="Xin Wang" uniqKey="Xin Wang" last="Xin Wang">XIN WANG</name><affiliation><inist:fA14 i1="02"><s1>Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Oishi, Kenichi" sort="Oishi, Kenichi" uniqKey="Oishi K" first="Kenichi" last="Oishi">Kenichi Oishi</name><affiliation><inist:fA14 i1="02"><s1>Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Brandt, Jason" sort="Brandt, Jason" uniqKey="Brandt J" first="Jason" last="Brandt">Jason Brandt</name><affiliation><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Department of Neurology, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>8 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Bassett, Susan S" sort="Bassett, Susan S" uniqKey="Bassett S" first="Susan S." last="Bassett">Susan S. Bassett</name><affiliation><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Redgrave, Graham W" sort="Redgrave, Graham W" uniqKey="Redgrave G" first="Graham W." last="Redgrave">Graham W. Redgrave</name><affiliation><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Margolis, Russell L" sort="Margolis, Russell L" uniqKey="Margolis R" first="Russell L." last="Margolis">Russell L. Margolis</name><affiliation><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Department of Neurology, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>8 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Van Zijl, Peter C M" sort="Van Zijl, Peter C M" uniqKey="Van Zijl P" first="Peter C. M." last="Van Zijl">Peter C. M. Van Zijl</name><affiliation><inist:fA14 i1="02"><s1>Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Barker, Peter B" sort="Barker, Peter B" uniqKey="Barker P" first="Peter B." last="Barker">Peter B. Barker</name><affiliation><inist:fA14 i1="02"><s1>Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ross, Christopher A" sort="Ross, Christopher A" uniqKey="Ross C" first="Christopher A." last="Ross">Christopher A. Ross</name><affiliation><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Department of Neurology, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>8 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="06"><s1>Department of Neuroscience and Pharmacology, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>14 aut.</sZ></inist:fA14></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="2012">2012</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>Cognition</term><term>Cognitive disorder</term><term>Degeneration</term><term>Encephalon</term><term>Glutamate</term><term>Huntington disease</term><term>Metabolite</term><term>Nervous system diseases</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Trouble cognitif</term><term>Chorée de Huntington</term><term>Dégénérescence</term><term>Pathologie du système nerveux</term><term>Encéphale</term><term>Métabolite</term><term>Glutamate</term><term>Cognition</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Huntington's disease (HD) is a neurodegenerative disorder characterized by early cognitive decline that progresses at later stages to dementia and severe movement disorder. HD is caused by a cytosine-adenine- guanine triplet-repeat expansion mutation in the Huntingtin gene, allowing early diagnosis by genetic testing. This study aimed to identify the relationship of N-acetylaspartate and other brain metabolites to cognitive function in HD-mutation carriers by using high-field-strength magnetic resonance spectroscopy (MRS) at 7 Tesla. Twelve individuals with the HD mutation in premanifest or early-stage disease versus 12 healthy controls underwent <sup>1</sup>H magnetic resonance spectroscopy (7.2 mL voxel in the posterior cingulate cortex) at 7 Tesla, and also T1-weighted structural magnetic resonance imaging. All participants received standardized tests of cognitive functioning including the Montreal Cognitive Assessment and standardized quantified neurological examination within an hour before scanning. Individuals with the HD mutation had significantly lower posterior cingulate cortex N-acetylaspartate (-9.6%, P =.02) and glutamate (-10.1 %, P = .02) levels than did controls. In contrast, in this small group, measures of brain morphology including striatal and ventricle volumes did not differ significantly. Linear regression with Montreal Cognitive Assessment scores revealed significant correlations with N-acetylaspartate (r<sup>2</sup> = 0.50, P = .01) and glutamate (NAA) (r<sup>2</sup> = 0.64, P = .002) in HD subjects. Our data suggest a relationship between reduced N-acetylaspartate and glutamate levels in the posterior cingulate cortex with cognitive decline in the early stages of HD. N-acetylaspartate and glutamate magnetic resonance spectroscopy signals of the posterior cingulate cortex region may serve as potential biomarkers of disease progression or treatment outcome in HD and other neurodegenerative disorders with early cognitive dysfunction, when structural brain changes are still minor.</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>27</s2></fA05><fA06><s2>7</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Brain Metabolite Alterations and Cognitive Dysfunction in Early Huntington's Disease</s1></fA08><fA11 i1="01" i2="1"><s1>UNSCHULD (Paul G.)</s1></fA11><fA11 i1="02" i2="1"><s1>EDDEN (Richard A. E.)</s1></fA11><fA11 i1="03" i2="1"><s1>CARASS (Aaron)</s1></fA11><fA11 i1="04" i2="1"><s1>XINYANG LIU</s1></fA11><fA11 i1="05" i2="1"><s1>SHANAHAN (Megan)</s1></fA11><fA11 i1="06" i2="1"><s1>XIN WANG</s1></fA11><fA11 i1="07" i2="1"><s1>OISHI (Kenichi)</s1></fA11><fA11 i1="08" i2="1"><s1>BRANDT (Jason)</s1></fA11><fA11 i1="09" i2="1"><s1>BASSETT (Susan S.)</s1></fA11><fA11 i1="10" i2="1"><s1>REDGRAVE (Graham W.)</s1></fA11><fA11 i1="11" i2="1"><s1>MARGOLIS (Russell L.)</s1></fA11><fA11 i1="12" i2="1"><s1>VAN ZIJL (Peter C. M.)</s1></fA11><fA11 i1="13" i2="1"><s1>BARKER (Peter B.)</s1></fA11><fA11 i1="14" i2="1"><s1>ROSS (Christopher A.)</s1></fA11><fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></fA14><fA14 i1="02"><s1>Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></fA14><fA14 i1="03"><s1>F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>13 aut.</sZ></fA14><fA14 i1="04"><s1>Brigham and Women's Hospital, Harvard Medical School</s1><s2>Boston, Massachusetts</s2><s3>USA</s3><sZ>4 aut.</sZ></fA14><fA14 i1="05"><s1>Department of Neurology, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>8 aut.</sZ><sZ>11 aut.</sZ><sZ>14 aut.</sZ></fA14><fA14 i1="06"><s1>Department of Neuroscience and Pharmacology, Johns Hopkins University School of Medicine</s1><s2>Baltimore, Maryland</s2><s3>USA</s3><sZ>14 aut.</sZ></fA14><fA20><s1>895-902</s1></fA20><fA21><s1>2012</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000508307110130</s5></fA43><fA44><s0>0000</s0><s1>© 2012 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>65 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>12-0280048</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) is a neurodegenerative disorder characterized by early cognitive decline that progresses at later stages to dementia and severe movement disorder. HD is caused by a cytosine-adenine- guanine triplet-repeat expansion mutation in the Huntingtin gene, allowing early diagnosis by genetic testing. This study aimed to identify the relationship of N-acetylaspartate and other brain metabolites to cognitive function in HD-mutation carriers by using high-field-strength magnetic resonance spectroscopy (MRS) at 7 Tesla. Twelve individuals with the HD mutation in premanifest or early-stage disease versus 12 healthy controls underwent <sup>1</sup>H magnetic resonance spectroscopy (7.2 mL voxel in the posterior cingulate cortex) at 7 Tesla, and also T1-weighted structural magnetic resonance imaging. All participants received standardized tests of cognitive functioning including the Montreal Cognitive Assessment and standardized quantified neurological examination within an hour before scanning. Individuals with the HD mutation had significantly lower posterior cingulate cortex N-acetylaspartate (-9.6%, P =.02) and glutamate (-10.1 %, P = .02) levels than did controls. In contrast, in this small group, measures of brain morphology including striatal and ventricle volumes did not differ significantly. Linear regression with Montreal Cognitive Assessment scores revealed significant correlations with N-acetylaspartate (r<sup>2</sup> = 0.50, P = .01) and glutamate (NAA) (r<sup>2</sup> = 0.64, P = .002) in HD subjects. Our data suggest a relationship between reduced N-acetylaspartate and glutamate levels in the posterior cingulate cortex with cognitive decline in the early stages of HD. N-acetylaspartate and glutamate magnetic resonance spectroscopy signals of the posterior cingulate cortex region may serve as potential biomarkers of disease progression or treatment outcome in HD and other neurodegenerative disorders with early cognitive dysfunction, when structural brain changes are still minor.</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>Trouble cognitif</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Cognitive disorder</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Trastorno cognitivo</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>Dégénérescence</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Degeneration</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Degeneración</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Encéphale</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Encephalon</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Encéfalo</s0><s5>09</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Métabolite</s0><s5>10</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Metabolite</s0><s5>10</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Metabolito</s0><s5>10</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Glutamate</s0><s2>NK</s2><s2>FX</s2><s5>11</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Glutamate</s0><s2>NK</s2><s2>FX</s2><s5>11</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Glutamato</s0><s2>NK</s2><s2>FX</s2><s5>11</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Cognition</s0><s5>12</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Cognition</s0><s5>12</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Cognición</s0><s5>12</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><fC07 i1="07" i2="X" l="FRE"><s0>Aminoacide excitateur</s0><s5>44</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Excitatory aminoacid</s0><s5>44</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Aminoácido excitador</s0><s5>44</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Neurotransmetteur</s0><s5>45</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Neurotransmitter</s0><s5>45</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Neurotransmisor</s0><s5>45</s5></fC07><fN21><s1>212</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 12-0280048 INIST</NO><ET>Brain Metabolite Alterations and Cognitive Dysfunction in Early Huntington's Disease</ET><AU>UNSCHULD (Paul G.); EDDEN (Richard A. E.); CARASS (Aaron); XINYANG LIU; SHANAHAN (Megan); XIN WANG; OISHI (Kenichi); BRANDT (Jason); BASSETT (Susan S.); REDGRAVE (Graham W.); MARGOLIS (Russell L.); VAN ZIJL (Peter C. M.); BARKER (Peter B.); ROSS (Christopher A.)</AU><AF>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine/Baltimore, Maryland/Etats-Unis (1 aut., 5 aut., 8 aut., 9 aut., 10 aut., 11 aut., 14 aut.); Russell H. Morgan Department of Radiology and Radiological Science, Division of MR Research, Johns Hopkins University School of Medicine/Baltimore, Maryland/Etats-Unis (2 aut., 3 aut., 6 aut., 7 aut., 12 aut., 13 aut.); F.M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute/Baltimore, Maryland/Etats-Unis (2 aut., 12 aut., 13 aut.); Brigham and Women's Hospital, Harvard Medical School/Boston, Massachusetts/Etats-Unis (4 aut.); Department of Neurology, Johns Hopkins University School of Medicine/Baltimore, Maryland/Etats-Unis (8 aut., 11 aut., 14 aut.); Department of Neuroscience and Pharmacology, Johns Hopkins University School of Medicine/Baltimore, Maryland/Etats-Unis (14 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2012; Vol. 27; No. 7; Pp. 895-902; Bibl. 65 ref.</SO><LA>Anglais</LA><EA>Huntington's disease (HD) is a neurodegenerative disorder characterized by early cognitive decline that progresses at later stages to dementia and severe movement disorder. HD is caused by a cytosine-adenine- guanine triplet-repeat expansion mutation in the Huntingtin gene, allowing early diagnosis by genetic testing. This study aimed to identify the relationship of N-acetylaspartate and other brain metabolites to cognitive function in HD-mutation carriers by using high-field-strength magnetic resonance spectroscopy (MRS) at 7 Tesla. Twelve individuals with the HD mutation in premanifest or early-stage disease versus 12 healthy controls underwent <sup>1</sup>H magnetic resonance spectroscopy (7.2 mL voxel in the posterior cingulate cortex) at 7 Tesla, and also T1-weighted structural magnetic resonance imaging. All participants received standardized tests of cognitive functioning including the Montreal Cognitive Assessment and standardized quantified neurological examination within an hour before scanning. Individuals with the HD mutation had significantly lower posterior cingulate cortex N-acetylaspartate (-9.6%, P =.02) and glutamate (-10.1 %, P = .02) levels than did controls. In contrast, in this small group, measures of brain morphology including striatal and ventricle volumes did not differ significantly. Linear regression with Montreal Cognitive Assessment scores revealed significant correlations with N-acetylaspartate (r<sup>2</sup> = 0.50, P = .01) and glutamate (NAA) (r<sup>2</sup> = 0.64, P = .002) in HD subjects. Our data suggest a relationship between reduced N-acetylaspartate and glutamate levels in the posterior cingulate cortex with cognitive decline in the early stages of HD. N-acetylaspartate and glutamate magnetic resonance spectroscopy signals of the posterior cingulate cortex region may serve as potential biomarkers of disease progression or treatment outcome in HD and other neurodegenerative disorders with early cognitive dysfunction, when structural brain changes are still minor.</EA><CC>002B17; 002B17G</CC><FD>Trouble cognitif; Chorée de Huntington; Dégénérescence; Pathologie du système nerveux; Encéphale; Métabolite; Glutamate; Cognition</FD><FG>Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Maladie héréditaire; Pathologie du système nerveux central; Aminoacide excitateur; Neurotransmetteur</FG><ED>Cognitive disorder; Huntington disease; Degeneration; Nervous system diseases; Encephalon; Metabolite; Glutamate; Cognition</ED><EG>Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Genetic disease; Central nervous system disease; Excitatory aminoacid; Neurotransmitter</EG><SD>Trastorno cognitivo; Corea Huntington; Degeneración; Sistema nervioso patología; Encéfalo; Metabolito; Glutamato; Cognición</SD><LO>INIST-20953.354000508307110130</LO><ID>12-0280048</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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