Evidence of thalamic dysfunction in Huntington disease by proton magnetic resonance spectroscopy.
Identifieur interne : 001D94 ( Ncbi/Checkpoint ); précédent : 001D93; suivant : 001D95Evidence of thalamic dysfunction in Huntington disease by proton magnetic resonance spectroscopy.
Auteurs : Heloísa H. Ruocco [Brésil] ; Iscia Lopes-Cendes ; Li M. Li ; Fernando CendesSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Adult, Age of Onset, Aged, Analysis of Variance, Aspartic Acid (analogs & derivatives), Aspartic Acid (metabolism), Creatine (metabolism), Female, Humans, Huntington Disease (pathology), Magnetic Resonance Spectroscopy (methods), Male, Middle Aged, Protons (diagnostic use), Thalamus (physiopathology), Thalamus (radionuclide imaging).
- MESH :
- chemical , analogs & derivatives : Aspartic Acid.
- chemical , diagnostic use : Protons.
- chemical , metabolism : Aspartic Acid, Creatine.
- methods : Magnetic Resonance Spectroscopy.
- pathology : Huntington Disease.
- physiopathology : Thalamus.
- radionuclide imaging : Thalamus.
- Adult, Age of Onset, Aged, Analysis of Variance, Female, Humans, Male, Middle Aged.
Abstract
Our objective was to investigate thalamic neuronal dysfunction in patients with Huntington disease (HD). We performed localized single-voxel proton magnetic resonance spectroscopy (MRS) of the thalamus in 22 HD patients and 25 healthy individuals. The mean age of patients was 48.5 years (ranging from 32 to 71 years). Age at onset varied between 20 and 66 years (mean 38.9 years). The expanded CAG repeat ranged from 40 to 52 (mean 45.2) CAGs. The mean age of control group was 35.4 years, ranging from 19 to 67 years. N-acetylaspartate (NAA) relative to creatine (NAA/Cr) values in the thalamus of HD patients were decreased when compared with controls (P = 0.0001). The spectroscopic findings were not correlated with motor impairment. However, there was a positive correlation between duration of disease and motor impairment (P = 0.02, r = 0.48), and a tendency for positive correlation between duration of disease and NAA/Cr (P = 0.059, r = 0.4). We found decreased NAA/Cr values in the thalamus of patients with HD, indicating neuronal loss or dysfunction. This is in agreement with previous studies that indicated the involvement of mitochondrial dysfunction in the neurodegenerative process of HD.
DOI: 10.1002/mds.21601
PubMed: 17702030
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Evidence of thalamic dysfunction in Huntington disease by proton magnetic resonance spectroscopy.</title><author><name sortKey="Ruocco, Heloisa H" sort="Ruocco, Heloisa H" uniqKey="Ruocco H" first="Heloísa H" last="Ruocco">Heloísa H. Ruocco</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurology, University of Campinas, Campinas, São Paulo, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Department of Neurology, University of Campinas, Campinas, São Paulo</wicri:regionArea><placeName><settlement type="city">São Paulo</settlement><region type="state">État de São Paulo</region></placeName></affiliation></author><author><name sortKey="Lopes Cendes, Iscia" sort="Lopes Cendes, Iscia" uniqKey="Lopes Cendes I" first="Iscia" last="Lopes-Cendes">Iscia Lopes-Cendes</name></author><author><name sortKey="Li, Li M" sort="Li, Li M" uniqKey="Li L" first="Li M" last="Li">Li M. Li</name></author><author><name sortKey="Cendes, Fernando" sort="Cendes, Fernando" uniqKey="Cendes F" first="Fernando" last="Cendes">Fernando Cendes</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="doi">10.1002/mds.21601</idno><idno type="RBID">pubmed:17702030</idno><idno type="pmid">17702030</idno><idno type="wicri:Area/PubMed/Corpus">002565</idno><idno type="wicri:Area/PubMed/Curation">002565</idno><idno type="wicri:Area/PubMed/Checkpoint">002825</idno><idno type="wicri:Area/Ncbi/Merge">001D94</idno><idno type="wicri:Area/Ncbi/Curation">001D94</idno><idno type="wicri:Area/Ncbi/Checkpoint">001D94</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Evidence of thalamic dysfunction in Huntington disease by proton magnetic resonance spectroscopy.</title><author><name sortKey="Ruocco, Heloisa H" sort="Ruocco, Heloisa H" uniqKey="Ruocco H" first="Heloísa H" last="Ruocco">Heloísa H. Ruocco</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurology, University of Campinas, Campinas, São Paulo, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Department of Neurology, University of Campinas, Campinas, São Paulo</wicri:regionArea><placeName><settlement type="city">São Paulo</settlement><region type="state">État de São Paulo</region></placeName></affiliation></author><author><name sortKey="Lopes Cendes, Iscia" sort="Lopes Cendes, Iscia" uniqKey="Lopes Cendes I" first="Iscia" last="Lopes-Cendes">Iscia Lopes-Cendes</name></author><author><name sortKey="Li, Li M" sort="Li, Li M" uniqKey="Li L" first="Li M" last="Li">Li M. Li</name></author><author><name sortKey="Cendes, Fernando" sort="Cendes, Fernando" uniqKey="Cendes F" first="Fernando" last="Cendes">Fernando Cendes</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Age of Onset</term><term>Aged</term><term>Analysis of Variance</term><term>Aspartic Acid (analogs & derivatives)</term><term>Aspartic Acid (metabolism)</term><term>Creatine (metabolism)</term><term>Female</term><term>Humans</term><term>Huntington Disease (pathology)</term><term>Magnetic Resonance Spectroscopy (methods)</term><term>Male</term><term>Middle Aged</term><term>Protons (diagnostic use)</term><term>Thalamus (physiopathology)</term><term>Thalamus (radionuclide imaging)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Aspartic Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Protons</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Aspartic Acid</term><term>Creatine</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Magnetic Resonance Spectroscopy</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Huntington Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Thalamus</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Thalamus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Age of Onset</term><term>Aged</term><term>Analysis of Variance</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Our objective was to investigate thalamic neuronal dysfunction in patients with Huntington disease (HD). We performed localized single-voxel proton magnetic resonance spectroscopy (MRS) of the thalamus in 22 HD patients and 25 healthy individuals. The mean age of patients was 48.5 years (ranging from 32 to 71 years). Age at onset varied between 20 and 66 years (mean 38.9 years). The expanded CAG repeat ranged from 40 to 52 (mean 45.2) CAGs. The mean age of control group was 35.4 years, ranging from 19 to 67 years. N-acetylaspartate (NAA) relative to creatine (NAA/Cr) values in the thalamus of HD patients were decreased when compared with controls (P = 0.0001). The spectroscopic findings were not correlated with motor impairment. However, there was a positive correlation between duration of disease and motor impairment (P = 0.02, r = 0.48), and a tendency for positive correlation between duration of disease and NAA/Cr (P = 0.059, r = 0.4). We found decreased NAA/Cr values in the thalamus of patients with HD, indicating neuronal loss or dysfunction. This is in agreement with previous studies that indicated the involvement of mitochondrial dysfunction in the neurodegenerative process of HD.</div></front></TEI><affiliations><list><country><li>Brésil</li></country><region><li>État de São Paulo</li></region><settlement><li>São Paulo</li></settlement></list><tree><noCountry><name sortKey="Cendes, Fernando" sort="Cendes, Fernando" uniqKey="Cendes F" first="Fernando" last="Cendes">Fernando Cendes</name><name sortKey="Li, Li M" sort="Li, Li M" uniqKey="Li L" first="Li M" last="Li">Li M. Li</name><name sortKey="Lopes Cendes, Iscia" sort="Lopes Cendes, Iscia" uniqKey="Lopes Cendes I" first="Iscia" last="Lopes-Cendes">Iscia Lopes-Cendes</name></noCountry><country name="Brésil"><region name="État de São Paulo"><name sortKey="Ruocco, Heloisa H" sort="Ruocco, Heloisa H" uniqKey="Ruocco H" first="Heloísa H" last="Ruocco">Heloísa H. Ruocco</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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