MovDisordV3, Main, Exploration, bibRecord, 001188

Brain Metabolite Alterations and Cognitive Dysfunction in Early Huntington's Disease

Identifieur interne : 001188 ( Main/Exploration ); précédent : 001187; suivant : 001189

Brain Metabolite Alterations and Cognitive Dysfunction in Early Huntington's Disease

Auteurs : Paul G. Unschuld [États-Unis] ; Richard A. E. Edden [États-Unis] ; Aaron Carass [États-Unis] ; XINYANG LIU [États-Unis] ; Megan Shanahan [États-Unis] ; XIN WANG [États-Unis] ; Kenichi Oishi [États-Unis] ; Jason Brandt [États-Unis] ; Susan S. Bassett [États-Unis] ; Graham W. Redgrave [États-Unis] ; Russell L. Margolis [États-Unis] ; Peter C. M. Van Zijl [États-Unis] ; Peter B. Barker [États-Unis] ; Christopher A. Ross [États-Unis]

Source :

Movement disorders [ 0885-3185 ] ; 2012.

RBID : Pascal:12-0280048

Descripteurs français

Pascal (Inist)
- Trouble cognitif, Chorée de Huntington, Dégénérescence, Pathologie du système nerveux, Encéphale, Métabolite, Glutamate, Cognition.

English descriptors

KwdEn :
- Adult, Analysis of Variance, Aspartic Acid (analogs & derivatives), Aspartic Acid (metabolism), Brain (metabolism), Brain (pathology), Cognition, Cognition Disorders (etiology), Cognitive disorder, Degeneration, Encephalon, Female, Glutamate, Glutamic Acid (metabolism), Humans, Huntington Disease (complications), Huntington Disease (genetics), Huntington Disease (pathology), Huntington disease, Magnetic Resonance Imaging, Magnetic Resonance Spectroscopy, Male, Metabolite, Middle Aged, Nervous system diseases, Neuropsychological Tests, Regression Analysis, Trinucleotide Repeat Expansion (genetics).
MESH :
- chemical , analogs & derivatives : Aspartic Acid.
- chemical , metabolism : Aspartic Acid, Glutamic Acid.
- complications : Huntington Disease.
- etiology : Cognition Disorders.
- genetics : Huntington Disease, Trinucleotide Repeat Expansion.
- metabolism : Brain.
- pathology : Brain, Huntington Disease.
- Adult, Analysis of Variance, Female, Humans, Magnetic Resonance Imaging, Magnetic Resonance Spectroscopy, Male, Middle Aged, Neuropsychological Tests, Regression Analysis.

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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3383395

Affiliations:

Le document en format XML

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<affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1>
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<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>
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<author><name sortKey="Barker, Peter B" sort="Barker, Peter B" uniqKey="Barker P" first="Peter B." last="Barker">Peter B. Barker</name>
<affiliation wicri:level="2"><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>
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<author><name sortKey="Ross, Christopher A" sort="Ross, Christopher A" uniqKey="Ross C" first="Christopher A." last="Ross">Christopher A. Ross</name>
<affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine</s1>
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<placeName><region type="state">Maryland</region>
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<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>Adult</term>
<term>Analysis of Variance</term>
<term>Aspartic Acid (analogs & derivatives)</term>
<term>Aspartic Acid (metabolism)</term>
<term>Brain (metabolism)</term>
<term>Brain (pathology)</term>
<term>Cognition</term>
<term>Cognition Disorders (etiology)</term>
<term>Cognitive disorder</term>
<term>Degeneration</term>
<term>Encephalon</term>
<term>Female</term>
<term>Glutamate</term>
<term>Glutamic Acid (metabolism)</term>
<term>Humans</term>
<term>Huntington Disease (complications)</term>
<term>Huntington Disease (genetics)</term>
<term>Huntington Disease (pathology)</term>
<term>Huntington disease</term>
<term>Magnetic Resonance Imaging</term>
<term>Magnetic Resonance Spectroscopy</term>
<term>Male</term>
<term>Metabolite</term>
<term>Middle Aged</term>
<term>Nervous system diseases</term>
<term>Neuropsychological Tests</term>
<term>Regression Analysis</term>
<term>Trinucleotide Repeat Expansion (genetics)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Aspartic Acid</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Aspartic Acid</term>
<term>Glutamic Acid</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Huntington Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Huntington Disease</term>
<term>Trinucleotide Repeat Expansion</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term>
<term>Huntington Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Analysis of Variance</term>
<term>Female</term>
<term>Humans</term>
<term>Magnetic Resonance Imaging</term>
<term>Magnetic Resonance Spectroscopy</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Neuropsychological Tests</term>
<term>Regression Analysis</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>
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</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>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Maryland</li>
<li>Massachusetts</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Maryland"><name sortKey="Unschuld, Paul G" sort="Unschuld, Paul G" uniqKey="Unschuld P" first="Paul G." last="Unschuld">Paul G. Unschuld</name>
</region>
<name sortKey="Barker, Peter B" sort="Barker, Peter B" uniqKey="Barker P" first="Peter B." last="Barker">Peter B. Barker</name>
<name sortKey="Barker, Peter B" sort="Barker, Peter B" uniqKey="Barker P" first="Peter B." last="Barker">Peter B. Barker</name>
<name sortKey="Bassett, Susan S" sort="Bassett, Susan S" uniqKey="Bassett S" first="Susan S." last="Bassett">Susan S. Bassett</name>
<name sortKey="Brandt, Jason" sort="Brandt, Jason" uniqKey="Brandt J" first="Jason" last="Brandt">Jason Brandt</name>
<name sortKey="Brandt, Jason" sort="Brandt, Jason" uniqKey="Brandt J" first="Jason" last="Brandt">Jason Brandt</name>
<name sortKey="Carass, Aaron" sort="Carass, Aaron" uniqKey="Carass A" first="Aaron" last="Carass">Aaron Carass</name>
<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>
<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>
<name sortKey="Margolis, Russell L" sort="Margolis, Russell L" uniqKey="Margolis R" first="Russell L." last="Margolis">Russell L. Margolis</name>
<name sortKey="Margolis, Russell L" sort="Margolis, Russell L" uniqKey="Margolis R" first="Russell L." last="Margolis">Russell L. Margolis</name>
<name sortKey="Oishi, Kenichi" sort="Oishi, Kenichi" uniqKey="Oishi K" first="Kenichi" last="Oishi">Kenichi Oishi</name>
<name sortKey="Redgrave, Graham W" sort="Redgrave, Graham W" uniqKey="Redgrave G" first="Graham W." last="Redgrave">Graham W. Redgrave</name>
<name sortKey="Ross, Christopher A" sort="Ross, Christopher A" uniqKey="Ross C" first="Christopher A." last="Ross">Christopher A. Ross</name>
<name sortKey="Ross, Christopher A" sort="Ross, Christopher A" uniqKey="Ross C" first="Christopher A." last="Ross">Christopher A. Ross</name>
<name sortKey="Ross, Christopher A" sort="Ross, Christopher A" uniqKey="Ross C" first="Christopher A." last="Ross">Christopher A. Ross</name>
<name sortKey="Shanahan, Megan" sort="Shanahan, Megan" uniqKey="Shanahan M" first="Megan" last="Shanahan">Megan Shanahan</name>
<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>
<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>
<name sortKey="Xin Wang" sort="Xin Wang" uniqKey="Xin Wang" last="Xin Wang">XIN WANG</name>
<name sortKey="Xinyang Liu" sort="Xinyang Liu" uniqKey="Xinyang Liu" last="Xinyang Liu">XINYANG LIU</name>
</country>
</tree>
</affiliations>
</record>

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Movement Disorders (revue)

Brain Metabolite Alterations and Cognitive Dysfunction in Early Huntington's Disease

Brain Metabolite Alterations and Cognitive Dysfunction in Early Huntington's Disease

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	Movement Disorders (revue)
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