Abnormal Response to Cortical Activation in Early Stages of Huntington Disease
Identifieur interne : 000152 ( PascalFrancis/Corpus ); précédent : 000151; suivant : 000153Abnormal Response to Cortical Activation in Early Stages of Huntington Disease
Auteurs : Fanny Mochel ; Tra-My N'Guyen ; Dinesh Deelchand ; Daisy Rinaldi ; Romain Valabregue ; Claire Wary ; Pierre G. Carlier ; Alexandra Durr ; Pierre-Gilles HenrySource :
- Movement disorders [ 0885-3185 ] ; 2012.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Background: We wished to identify noninvasive in vivo biomarkers of brain energy deficit in Huntington disease. Methods: We studied 15 early affected patients (mean motor United Huntington Disease Rating Scale, 18 ± 9) and 15 age- and sex-matched controls. We coupled 31phosphorus nuclear magnetic resonance spectroscopy with activation of the occipital cortex in order to measure the relative concentrations of adenosine triphosphate, phosphocreatine, and inorganic phosphate before, during, and after visual stimulation. Results: In controls, we observed an 11% increase in the inorganic phosphate/phosphocreatine ratio (P = .024) and a 13% increase in the inorganic phosphate/ adenosine triphosphate ratio (P = .016) during brain activation, reflecting increased adenosine diphosphate concentrations. Subsequently, controls had a return to baseline levels during recovery (P = .012 and .022, respectively). In contrast, both ratios were unchanged in patients during and after visual stimulation. Conclusions: 31Phosphorus nuclear magnetic resonance spectroscopy could provide functional biomarkers of brain energy deficit to monitor therapeutic efficacy in Huntington disease.
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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 12-0280059 INIST |
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ET : | Abnormal Response to Cortical Activation in Early Stages of Huntington Disease |
AU : | MOCHEL (Fanny); N'GUYEN (Tra-My); DEELCHAND (Dinesh); RINALDI (Daisy); VALABREGUE (Romain); WARY (Claire); CARLIER (Pierre G.); DURR (Alexandra); HENRY (Pierre-Gilles) |
AF : | INSERM UMR S975, Institut du Cerveau et de la Moelle, Hôpital La Salpêtrière/Paris/France (1 aut., 2 aut., 4 aut., 5 aut., 8 aut.); AP-HP, Département de Génétique, Hôpital La Salpêtrière/Paris/France (1 aut., 8 aut.); Unité Fonctionnelle Neurométabolique, Hôpital La Salpêtrière/Paris/France (1 aut., 4 aut.); Université Pierre et Marie Curie/Paris/France (1 aut., 5 aut., 6 aut., 7 aut.); University of Minnesota, Center for Magnetic Resonance Research, 2021 6th Street SE/Minneapolis, Minnesota/Etats-Unis (3 aut., 9 aut.); Institute du Cerveau et de la Moelle, Centre de Neurolmagerie de Recherche, Hôpital La Salpêtrière/Paris/France (5 aut.); Institut de Myologie, Laboratoire de RMN, Hôpital La Salpêtrière/Paris/France (6 aut., 7 aut.); CLA, I2BM, MIRCen, IdM NMR Laboratory/Paris/France (6 aut., 7 aut.) |
DT : | Publication en série; Courte communication, note brève; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2012; Vol. 27; No. 7; Pp. 907-910; Bibl. 17 ref. |
LA : | Anglais |
EA : | Background: We wished to identify noninvasive in vivo biomarkers of brain energy deficit in Huntington disease. Methods: We studied 15 early affected patients (mean motor United Huntington Disease Rating Scale, 18 ± 9) and 15 age- and sex-matched controls. We coupled 31phosphorus nuclear magnetic resonance spectroscopy with activation of the occipital cortex in order to measure the relative concentrations of adenosine triphosphate, phosphocreatine, and inorganic phosphate before, during, and after visual stimulation. Results: In controls, we observed an 11% increase in the inorganic phosphate/phosphocreatine ratio (P = .024) and a 13% increase in the inorganic phosphate/ adenosine triphosphate ratio (P = .016) during brain activation, reflecting increased adenosine diphosphate concentrations. Subsequently, controls had a return to baseline levels during recovery (P = .012 and .022, respectively). In contrast, both ratios were unchanged in patients during and after visual stimulation. Conclusions: 31Phosphorus nuclear magnetic resonance spectroscopy could provide functional biomarkers of brain energy deficit to monitor therapeutic efficacy in Huntington disease. |
CC : | 002B17; 002B17G |
FD : | Chorée de Huntington; Pathologie du système nerveux; Stade précoce; Spectrométrie; Métabolisme énergétique |
FG : | Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Maladie héréditaire; Pathologie du système nerveux central |
ED : | Huntington disease; Nervous system diseases; Early stage; Spectrometry; Energy metabolism |
EG : | Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Genetic disease; Central nervous system disease |
SD : | Corea Huntington; Sistema nervioso patología; Estadio precoz; Espectrometría; Metabolismo energético |
LO : | INIST-20953.354000508307110150 |
ID : | 12-0280059 |
Links to Exploration step
Pascal:12-0280059Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Abnormal Response to Cortical Activation in Early Stages of Huntington Disease</title>
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<author><name sortKey="Rinaldi, Daisy" sort="Rinaldi, Daisy" uniqKey="Rinaldi D" first="Daisy" last="Rinaldi">Daisy Rinaldi</name>
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<author><name sortKey="Wary, Claire" sort="Wary, Claire" uniqKey="Wary C" first="Claire" last="Wary">Claire Wary</name>
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<s3>FRA</s3>
<sZ>6 aut.</sZ>
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<author><name sortKey="Durr, Alexandra" sort="Durr, Alexandra" uniqKey="Durr A" first="Alexandra" last="Durr">Alexandra Durr</name>
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<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
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<sZ>1 aut.</sZ>
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<author><name sortKey="Henry, Pierre Gilles" sort="Henry, Pierre Gilles" uniqKey="Henry P" first="Pierre-Gilles" last="Henry">Pierre-Gilles Henry</name>
<affiliation><inist:fA14 i1="05"><s1>University of Minnesota, Center for Magnetic Resonance Research, 2021 6th Street SE</s1>
<s2>Minneapolis, Minnesota</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
<sZ>9 aut.</sZ>
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</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>
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<seriesStmt><title level="j" type="main">Movement disorders</title>
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<idno type="ISSN">0885-3185</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Early stage</term>
<term>Energy metabolism</term>
<term>Huntington disease</term>
<term>Nervous system diseases</term>
<term>Spectrometry</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Chorée de Huntington</term>
<term>Pathologie du système nerveux</term>
<term>Stade précoce</term>
<term>Spectrométrie</term>
<term>Métabolisme énergétique</term>
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</teiHeader>
<front><div type="abstract" xml:lang="en">Background: We wished to identify noninvasive in vivo biomarkers of brain energy deficit in Huntington disease. Methods: We studied 15 early affected patients (mean motor United Huntington Disease Rating Scale, 18 ± 9) and 15 age- and sex-matched controls. We coupled <sup>31</sup>
phosphorus nuclear magnetic resonance spectroscopy with activation of the occipital cortex in order to measure the relative concentrations of adenosine triphosphate, phosphocreatine, and inorganic phosphate before, during, and after visual stimulation. Results: In controls, we observed an 11% increase in the inorganic phosphate/phosphocreatine ratio (P = .024) and a 13% increase in the inorganic phosphate/ adenosine triphosphate ratio (P = .016) during brain activation, reflecting increased adenosine diphosphate concentrations. Subsequently, controls had a return to baseline levels during recovery (P = .012 and .022, respectively). In contrast, both ratios were unchanged in patients during and after visual stimulation. Conclusions: <sup>31</sup>
Phosphorus nuclear magnetic resonance spectroscopy could provide functional biomarkers of brain energy deficit to monitor therapeutic efficacy in Huntington disease.</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>Abnormal Response to Cortical Activation in Early Stages of Huntington Disease</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>MOCHEL (Fanny)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>N'GUYEN (Tra-My)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>DEELCHAND (Dinesh)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>RINALDI (Daisy)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>VALABREGUE (Romain)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>WARY (Claire)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>CARLIER (Pierre G.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>DURR (Alexandra)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>HENRY (Pierre-Gilles)</s1>
</fA11>
<fA14 i1="01"><s1>INSERM UMR S975, Institut du Cerveau et de la Moelle, Hôpital La Salpêtrière</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>AP-HP, Département de Génétique, Hôpital La Salpêtrière</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Unité Fonctionnelle Neurométabolique, Hôpital La Salpêtrière</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Université Pierre et Marie Curie</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>University of Minnesota, Center for Magnetic Resonance Research, 2021 6th Street SE</s1>
<s2>Minneapolis, Minnesota</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Institute du Cerveau et de la Moelle, Centre de Neurolmagerie de Recherche, Hôpital La Salpêtrière</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Institut de Myologie, Laboratoire de RMN, Hôpital La Salpêtrière</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>CLA, I<sup>2</sup>
BM, MIRCen, IdM NMR Laboratory</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA20><s1>907-910</s1>
</fA20>
<fA21><s1>2012</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000508307110150</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2012 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>17 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>12-0280059</s0>
</fA47>
<fA60><s1>P</s1>
<s3>CC</s3>
</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>Background: We wished to identify noninvasive in vivo biomarkers of brain energy deficit in Huntington disease. Methods: We studied 15 early affected patients (mean motor United Huntington Disease Rating Scale, 18 ± 9) and 15 age- and sex-matched controls. We coupled <sup>31</sup>
phosphorus nuclear magnetic resonance spectroscopy with activation of the occipital cortex in order to measure the relative concentrations of adenosine triphosphate, phosphocreatine, and inorganic phosphate before, during, and after visual stimulation. Results: In controls, we observed an 11% increase in the inorganic phosphate/phosphocreatine ratio (P = .024) and a 13% increase in the inorganic phosphate/ adenosine triphosphate ratio (P = .016) during brain activation, reflecting increased adenosine diphosphate concentrations. Subsequently, controls had a return to baseline levels during recovery (P = .012 and .022, respectively). In contrast, both ratios were unchanged in patients during and after visual stimulation. Conclusions: <sup>31</sup>
Phosphorus nuclear magnetic resonance spectroscopy could provide functional biomarkers of brain energy deficit to monitor therapeutic efficacy in Huntington disease.</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>Chorée de Huntington</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Huntington disease</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Corea Huntington</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Stade précoce</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Early stage</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Estadio precoz</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Spectrométrie</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Spectrometry</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Espectrometría</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Métabolisme énergétique</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Energy metabolism</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Metabolismo energético</s0>
<s5>11</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Maladie héréditaire</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Genetic disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>41</s5>
</fC07>
<fN21><s1>212</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
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<server><NO>PASCAL 12-0280059 INIST</NO>
<ET>Abnormal Response to Cortical Activation in Early Stages of Huntington Disease</ET>
<AU>MOCHEL (Fanny); N'GUYEN (Tra-My); DEELCHAND (Dinesh); RINALDI (Daisy); VALABREGUE (Romain); WARY (Claire); CARLIER (Pierre G.); DURR (Alexandra); HENRY (Pierre-Gilles)</AU>
<AF>INSERM UMR S975, Institut du Cerveau et de la Moelle, Hôpital La Salpêtrière/Paris/France (1 aut., 2 aut., 4 aut., 5 aut., 8 aut.); AP-HP, Département de Génétique, Hôpital La Salpêtrière/Paris/France (1 aut., 8 aut.); Unité Fonctionnelle Neurométabolique, Hôpital La Salpêtrière/Paris/France (1 aut., 4 aut.); Université Pierre et Marie Curie/Paris/France (1 aut., 5 aut., 6 aut., 7 aut.); University of Minnesota, Center for Magnetic Resonance Research, 2021 6th Street SE/Minneapolis, Minnesota/Etats-Unis (3 aut., 9 aut.); Institute du Cerveau et de la Moelle, Centre de Neurolmagerie de Recherche, Hôpital La Salpêtrière/Paris/France (5 aut.); Institut de Myologie, Laboratoire de RMN, Hôpital La Salpêtrière/Paris/France (6 aut., 7 aut.); CLA, I<sup>2</sup>
BM, MIRCen, IdM NMR Laboratory/Paris/France (6 aut., 7 aut.)</AF>
<DT>Publication en série; Courte communication, note brève; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2012; Vol. 27; No. 7; Pp. 907-910; Bibl. 17 ref.</SO>
<LA>Anglais</LA>
<EA>Background: We wished to identify noninvasive in vivo biomarkers of brain energy deficit in Huntington disease. Methods: We studied 15 early affected patients (mean motor United Huntington Disease Rating Scale, 18 ± 9) and 15 age- and sex-matched controls. We coupled <sup>31</sup>
phosphorus nuclear magnetic resonance spectroscopy with activation of the occipital cortex in order to measure the relative concentrations of adenosine triphosphate, phosphocreatine, and inorganic phosphate before, during, and after visual stimulation. Results: In controls, we observed an 11% increase in the inorganic phosphate/phosphocreatine ratio (P = .024) and a 13% increase in the inorganic phosphate/ adenosine triphosphate ratio (P = .016) during brain activation, reflecting increased adenosine diphosphate concentrations. Subsequently, controls had a return to baseline levels during recovery (P = .012 and .022, respectively). In contrast, both ratios were unchanged in patients during and after visual stimulation. Conclusions: <sup>31</sup>
Phosphorus nuclear magnetic resonance spectroscopy could provide functional biomarkers of brain energy deficit to monitor therapeutic efficacy in Huntington disease.</EA>
<CC>002B17; 002B17G</CC>
<FD>Chorée de Huntington; Pathologie du système nerveux; Stade précoce; Spectrométrie; Métabolisme énergétique</FD>
<FG>Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Maladie héréditaire; Pathologie du système nerveux central</FG>
<ED>Huntington disease; Nervous system diseases; Early stage; Spectrometry; Energy metabolism</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Genetic disease; Central nervous system disease</EG>
<SD>Corea Huntington; Sistema nervioso patología; Estadio precoz; Espectrometría; Metabolismo energético</SD>
<LO>INIST-20953.354000508307110150</LO>
<ID>12-0280059</ID>
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