Brain metabolite alterations and cognitive dysfunction in early Huntington's disease.
Identifieur interne : 000D62 ( PubMed/Curation ); précédent : 000D61; suivant : 000D63Brain metabolite alterations and cognitive dysfunction in early Huntington's disease.
Auteurs : Paul G. Unschuld [États-Unis] ; 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 : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2012.
English descriptors
- KwdEn :
- Adult, Analysis of Variance, Aspartic Acid (analogs & derivatives), Aspartic Acid (metabolism), Brain (metabolism), Brain (pathology), Cognition Disorders (etiology), Female, Glutamic Acid (metabolism), Humans, Huntington Disease (complications), Huntington Disease (genetics), Huntington Disease (pathology), Magnetic Resonance Imaging, Magnetic Resonance Spectroscopy, Male, Middle Aged, 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 (1)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(2) = 0.50, P = .01) and glutamate (NAA) (r(2) = 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.
DOI: 10.1002/mds.25010
PubMed: 22649062
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Edden</name></author><author><name sortKey="Carass, Aaron" sort="Carass, Aaron" uniqKey="Carass A" first="Aaron" last="Carass">Aaron Carass</name></author><author><name sortKey="Liu, Xinyang" sort="Liu, Xinyang" uniqKey="Liu X" first="Xinyang" last="Liu">Xinyang Liu</name></author><author><name sortKey="Shanahan, Megan" sort="Shanahan, Megan" uniqKey="Shanahan M" first="Megan" last="Shanahan">Megan Shanahan</name></author><author><name sortKey="Wang, Xin" sort="Wang, Xin" uniqKey="Wang X" first="Xin" last="Wang">Xin Wang</name></author><author><name sortKey="Oishi, Kenichi" sort="Oishi, Kenichi" uniqKey="Oishi K" first="Kenichi" last="Oishi">Kenichi Oishi</name></author><author><name sortKey="Brandt, Jason" sort="Brandt, Jason" uniqKey="Brandt J" first="Jason" last="Brandt">Jason Brandt</name></author><author><name sortKey="Bassett, Susan S" sort="Bassett, Susan S" uniqKey="Bassett S" first="Susan S" last="Bassett">Susan S. 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Unschuld</name><affiliation wicri:level="1"><nlm:affiliation>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA. unschuld@jhmi.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287</wicri:regionArea></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></author><author><name sortKey="Carass, Aaron" sort="Carass, Aaron" uniqKey="Carass A" first="Aaron" last="Carass">Aaron Carass</name></author><author><name sortKey="Liu, Xinyang" sort="Liu, Xinyang" uniqKey="Liu X" first="Xinyang" last="Liu">Xinyang Liu</name></author><author><name sortKey="Shanahan, Megan" sort="Shanahan, Megan" uniqKey="Shanahan M" first="Megan" last="Shanahan">Megan Shanahan</name></author><author><name sortKey="Wang, Xin" sort="Wang, Xin" uniqKey="Wang X" first="Xin" last="Wang">Xin Wang</name></author><author><name sortKey="Oishi, Kenichi" sort="Oishi, Kenichi" uniqKey="Oishi K" first="Kenichi" last="Oishi">Kenichi Oishi</name></author><author><name sortKey="Brandt, Jason" sort="Brandt, Jason" uniqKey="Brandt J" first="Jason" last="Brandt">Jason Brandt</name></author><author><name sortKey="Bassett, Susan S" sort="Bassett, Susan S" uniqKey="Bassett S" first="Susan S" last="Bassett">Susan S. Bassett</name></author><author><name sortKey="Redgrave, Graham W" sort="Redgrave, Graham W" uniqKey="Redgrave G" first="Graham W" last="Redgrave">Graham W. Redgrave</name></author><author><name sortKey="Margolis, Russell L" sort="Margolis, Russell L" uniqKey="Margolis R" first="Russell L" last="Margolis">Russell L. Margolis</name></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></author><author><name sortKey="Barker, Peter B" sort="Barker, Peter B" uniqKey="Barker P" first="Peter B" last="Barker">Peter B. Barker</name></author><author><name sortKey="Ross, Christopher A" sort="Ross, Christopher A" uniqKey="Ross C" first="Christopher A" last="Ross">Christopher A. Ross</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="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></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 Disorders (etiology)</term><term>Female</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>Magnetic Resonance Imaging</term><term>Magnetic Resonance Spectroscopy</term><term>Male</term><term>Middle Aged</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></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 (1)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(2) = 0.50, P = .01) and glutamate (NAA) (r(2) = 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><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">22649062</PMID><DateCreated><Year>2012</Year><Month>06</Month><Day>25</Day></DateCreated><DateCompleted><Year>2012</Year><Month>11</Month><Day>13</Day></DateCompleted><DateRevised><Year>2014</Year><Month>10</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>7</Issue><PubDate><Year>2012</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Brain metabolite alterations and cognitive dysfunction in early Huntington's disease.</ArticleTitle><Pagination><MedlinePgn>895-902</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25010</ELocationID><Abstract><AbstractText>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 (1)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(2) = 0.50, P = .01) and glutamate (NAA) (r(2) = 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.</AbstractText><CopyrightInformation>Copyright © 2012 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Unschuld</LastName><ForeName>Paul G</ForeName><Initials>PG</Initials><AffiliationInfo><Affiliation>Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA. unschuld@jhmi.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Edden</LastName><ForeName>Richard A E</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Carass</LastName><ForeName>Aaron</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Xinyang</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Shanahan</LastName><ForeName>Megan</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xin</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Oishi</LastName><ForeName>Kenichi</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Brandt</LastName><ForeName>Jason</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Bassett</LastName><ForeName>Susan S</ForeName><Initials>SS</Initials></Author><Author ValidYN="Y"><LastName>Redgrave</LastName><ForeName>Graham W</ForeName><Initials>GW</Initials></Author><Author ValidYN="Y"><LastName>Margolis</LastName><ForeName>Russell L</ForeName><Initials>RL</Initials></Author><Author ValidYN="Y"><LastName>van Zijl</LastName><ForeName>Peter C M</ForeName><Initials>PC</Initials></Author><Author ValidYN="Y"><LastName>Barker</LastName><ForeName>Peter B</ForeName><Initials>PB</Initials></Author><Author ValidYN="Y"><LastName>Ross</LastName><ForeName>Christopher A</ForeName><Initials>CA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NS16375</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41 EB015909</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41-RR015241</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 NS016375</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 NS016375-30S2</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50AG005146</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 MH015330</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 MH015330-35</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32MH015330</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH 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>2012</Year><Month>05</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>30KYC7MIAI</RegistryNumber><NameOfSubstance UI="D001224">Aspartic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>3KX376GY7L</RegistryNumber><NameOfSubstance UI="D018698">Glutamic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>997-55-7</RegistryNumber><NameOfSubstance UI="C000179">N-acetylaspartate</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>IEEE Trans Med Imaging. 2007 Apr;26(4):487-96</RefSource><PMID Version="1">17427736</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res. 2007 Sep 7;1168:67-71</RefSource><PMID Version="1">17707354</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Med Res. 2008 Apr;39(3):265-76</RefSource><PMID 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UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003072">Cognition Disorders</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000209">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018698">Glutamic Acid</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006816">Huntington Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName 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Source="NLM">PMC3383395</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2011</Year><Month>10</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2012</Year><Month>1</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>3</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2012</Year><Month>5</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>11</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.25010</ArticleId><ArticleId 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