MovDisordV3, PascalFrancis, Curation, bibRecord, 002B62

Abnormal Response to Cortical Activation in Early Stages of Huntington Disease

Identifieur interne : 002B62 ( PascalFrancis/Curation ); précédent : 002B61; suivant : 002B63

Abnormal Response to Cortical Activation in Early Stages of Huntington Disease

Auteurs : Fanny Mochel [France] ; Tra-My N'Guyen [France] ; Dinesh Deelchand [États-Unis] ; Daisy Rinaldi [France] ; Romain Valabregue [France] ; Claire Wary [France] ; Pierre G. Carlier [France] ; Alexandra Durr [France] ; Pierre-Gilles Henry [États-Unis]

Source :

Movement disorders [ 0885-3185 ] ; 2012.

RBID : Pascal:12-0280059

Descripteurs français

Pascal (Inist)
- Chorée de Huntington, Pathologie du système nerveux, Stade précoce, Spectrométrie, Métabolisme énergétique.
Wicri :
- topic : Spectrométrie.

English descriptors

KwdEn :
- Early stage, Energy metabolism, Huntington disease, Nervous system diseases, Spectrometry.

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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A11	`02`	`1`		`@1 N'GUYEN (Tra-My)`
A11	`03`	`1`		`@1 DEELCHAND (Dinesh)`
A11	`04`	`1`		`@1 RINALDI (Daisy)`
A11	`05`	`1`		`@1 VALABREGUE (Romain)`
A11	`06`	`1`		`@1 WARY (Claire)`
A11	`07`	`1`		`@1 CARLIER (Pierre G.)`
A11	`08`	`1`		`@1 DURR (Alexandra)`
A11	`09`	`1`		`@1 HENRY (Pierre-Gilles)`
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A14	`05`			`@1 University of Minnesota, Center for Magnetic Resonance Research, 2021 6th Street SE @2 Minneapolis, Minnesota @3 USA @Z 3 aut. @Z 9 aut.`
A14	`06`			`@1 Institute du Cerveau et de la Moelle, Centre de Neurolmagerie de Recherche, Hôpital La Salpêtrière @2 Paris @3 FRA @Z 5 aut.`
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C01	`01`		`ENG`	@0 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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C03	`05`	`X`	`FRE`	`@0 Métabolisme énergétique @5 11`
C03	`05`	`X`	`ENG`	`@0 Energy metabolism @5 11`
C03	`05`	`X`	`SPA`	`@0 Metabolismo energético @5 11`
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C07	`04`	`X`	`FRE`	`@0 Maladie héréditaire @5 40`
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Pascal:12-0280059

Le 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>
<author><name sortKey="Mochel, Fanny" sort="Mochel, Fanny" uniqKey="Mochel F" first="Fanny" last="Mochel">Fanny Mochel</name>
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<author><name sortKey="N Guyen, Tra My" sort="N Guyen, Tra My" uniqKey="N Guyen T" first="Tra-My" last="N'Guyen">Tra-My N'Guyen</name>
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<author><name sortKey="Deelchand, Dinesh" sort="Deelchand, Dinesh" uniqKey="Deelchand D" first="Dinesh" last="Deelchand">Dinesh Deelchand</name>
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<author><name sortKey="Rinaldi, Daisy" sort="Rinaldi, Daisy" uniqKey="Rinaldi D" first="Daisy" last="Rinaldi">Daisy Rinaldi</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>INSERM UMR S975, Institut du Cerveau et de la Moelle, Hôpital La Salpêtrière</s1>
<s2>Paris</s2>
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<sZ>1 aut.</sZ>
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</inist:fA14>
<country>France</country>
</affiliation>
<affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Unité Fonctionnelle Neurométabolique, Hôpital La Salpêtrière</s1>
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<author><name sortKey="Valabregue, Romain" sort="Valabregue, Romain" uniqKey="Valabregue R" first="Romain" last="Valabregue">Romain Valabregue</name>
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<affiliation wicri:level="1"><inist: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>
</inist:fA14>
<country>France</country>
</affiliation>
</author>
<author><name sortKey="Wary, Claire" sort="Wary, Claire" uniqKey="Wary C" first="Claire" last="Wary">Claire Wary</name>
<affiliation wicri:level="1"><inist: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>
</inist:fA14>
<country>France</country>
</affiliation>
<affiliation wicri:level="1"><inist: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>
</inist:fA14>
<country>France</country>
</affiliation>
<affiliation wicri:level="1"><inist: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>
</inist:fA14>
<country>France</country>
</affiliation>
</author>
<author><name sortKey="Carlier, Pierre G" sort="Carlier, Pierre G" uniqKey="Carlier P" first="Pierre G." last="Carlier">Pierre G. Carlier</name>
<affiliation wicri:level="1"><inist: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>
</inist:fA14>
<country>France</country>
</affiliation>
<affiliation wicri:level="1"><inist: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>
</inist:fA14>
<country>France</country>
</affiliation>
<affiliation wicri:level="1"><inist: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>
</inist:fA14>
<country>France</country>
</affiliation>
</author>
<author><name sortKey="Durr, Alexandra" sort="Durr, Alexandra" uniqKey="Durr A" first="Alexandra" last="Durr">Alexandra Durr</name>
<affiliation wicri:level="1"><inist: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>
</inist:fA14>
<country>France</country>
</affiliation>
<affiliation wicri:level="1"><inist: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>
</inist:fA14>
<country>France</country>
</affiliation>
</author>
<author><name sortKey="Henry, Pierre Gilles" sort="Henry, Pierre Gilles" uniqKey="Henry P" first="Pierre-Gilles" last="Henry">Pierre-Gilles Henry</name>
<affiliation wicri:level="1"><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>
</inist:fA14>
<country>États-Unis</country>
</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>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>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Spectrométrie</term>
</keywords>
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<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>
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</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>
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<s5>354000508307110150</s5>
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<s1>© 2012 INIST-CNRS. All rights reserved.</s1>
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</fA45>
<fA47 i1="01" i2="1"><s0>12-0280059</s0>
</fA47>
<fA60><s1>P</s1>
<s3>CC</s3>
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<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>
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<s5>02</s5>
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<s5>09</s5>
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<s5>09</s5>
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<s5>09</s5>
</fC03>
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<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>
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<s5>11</s5>
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<fC03 i1="05" i2="X" l="SPA"><s0>Metabolismo energético</s0>
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<fC07 i1="01" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
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</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
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<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
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<s5>38</s5>
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<s5>39</s5>
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<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>39</s5>
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<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>39</s5>
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<fC07 i1="04" i2="X" l="FRE"><s0>Maladie héréditaire</s0>
<s5>40</s5>
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<s5>40</s5>
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<s5>40</s5>
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<s5>41</s5>
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<s5>41</s5>
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<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>
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</pA>
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	Movement Disorders (revue)
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Movement Disorders (revue)

Abnormal Response to Cortical Activation in Early Stages of Huntington Disease

Abnormal Response to Cortical Activation in Early Stages of Huntington Disease

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