MovDisordV3, PascalFrancis, Curation, bibRecord, 002384

Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism

Identifieur interne : 002384 ( PascalFrancis/Curation ); précédent : 002383; suivant : 002385

Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism

Auteurs : Satoshi Kono [Japon] ; Yasuomi Ouchi [Japon] ; Tatsuhiro Terada [Japon] ; Hiroyuki Ida [Japon] ; Makiko Suzuki [Japon] ; Hiroaki Miyajima [Japon]

Source :

Movement disorders [ 0885-3185 ] ; 2010.

RBID : Pascal:10-0446278

Descripteurs français

Pascal (Inist)
- Parkinsonisme, Maladie de Parkinson, Pathologie du système nerveux, Imagerie fonctionnelle, Encéphale, Mutation, Porteur, Tomoscintigraphie, Tomographie par émission de positons, Glucose(2-désoxy-2-fluor), Raclopride.

English descriptors

KwdEn :
- 2-deoxy-2-fluoroglucose, Carrier, Emission tomography, Encephalon, Functional imaging, Mutation, Nervous system diseases, Parkinson disease, Parkinsonism, Positron emission tomography, Raclopride.

Abstract

Mutations in the glucocerebrosidase gene (GBA) increase the risk for Parkinson's disease and are also associated with an earlier onset of the disease and an akinetic parkinsonian phenotype. To investigate the underlying pathogenesis of this condition, we assessed cerebral metabolism using positron emission tomography (PET) in GBA mutation carriers with and without parkinsonism. [¹⁸F]-fluorodeoxyglucose (FDG)-PET using a three-dimensional stereotactic surface projection analysis was used to measure the cerebral metabolic rates of glucose (CMRGlc) in a patient with parkinsonism and Gaucher disease (GD) and five subjects with a heterozygous GBA mutation, including three patients with parkinsonism and three asymptomatic carriers in comparison to 10 healthy controls in the same age range. Dopaminergic neuronal activity was investigated using [¹¹C] CFT- and [¹¹C] raclopride-PET. All GBA mutation carriers displayed a significant CMRGlc decrease in the supplemental motor area (SMA). The carriers with parkinsonism showed additional hypometabolism in the parietooccipital cortices. The CFT and raclopride PET images in the asymptomatic carriers demonstrated the CFT binding to be within normal values in the putamen and a significant increase was observed in the caudate nucleus while raclopride binding in the striatum was in the normal range. An advanced parkinsonian carrier showed decreased CFT binding and increased raclopride binding in the striatum. The decreased CMRGlc in the SMA was characteristic of the GBA mutation carriers. The hypometabolism in the SMA may, therefore, be involved in the clinical characteristics of parkinsonism associated with GBA mutations when the carriers manifest parkinsonism.

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A03		`1`		`@0 Mov. disord.`
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A08	`01`	`1`	`ENG`	`@1 Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism`
A11	`01`	`1`		`@1 KONO (Satoshi)`
A11	`02`	`1`		`@1 OUCHI (Yasuomi)`
A11	`03`	`1`		`@1 TERADA (Tatsuhiro)`
A11	`04`	`1`		`@1 IDA (Hiroyuki)`
A11	`05`	`1`		`@1 SUZUKI (Makiko)`
A11	`06`	`1`		`@1 MIYAJIMA (Hiroaki)`
A14	`01`			`@1 Department of Medicine, Hamamatsu University School of Medicine @2 Hamamatsu @3 JPN @Z 1 aut. @Z 3 aut. @Z 5 aut. @Z 6 aut.`
A14	`02`			`@1 Laboratory of Human Brain Imaging Research, Molecular Imaging Frontier Research Center, Hamamatsu University School of Medicine @2 Hamamatsu @3 JPN @Z 2 aut.`
A14	`03`			`@1 Department of Pediatrics, Jikei University School of Medicine @2 Tokyo @3 JPN @Z 4 aut.`
A20				`@1 1823-1829`
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A44				`@0 0000 @1 © 2010 INIST-CNRS. All rights reserved.`
A45				`@0 35 ref.`
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A61				`@0 A`
A64	`01`	`1`		`@0 Movement disorders`
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C01	`01`		`ENG`	@0 Mutations in the glucocerebrosidase gene (GBA) increase the risk for Parkinson's disease and are also associated with an earlier onset of the disease and an akinetic parkinsonian phenotype. To investigate the underlying pathogenesis of this condition, we assessed cerebral metabolism using positron emission tomography (PET) in GBA mutation carriers with and without parkinsonism. [¹⁸F]-fluorodeoxyglucose (FDG)-PET using a three-dimensional stereotactic surface projection analysis was used to measure the cerebral metabolic rates of glucose (CMRGlc) in a patient with parkinsonism and Gaucher disease (GD) and five subjects with a heterozygous GBA mutation, including three patients with parkinsonism and three asymptomatic carriers in comparison to 10 healthy controls in the same age range. Dopaminergic neuronal activity was investigated using [¹¹C] CFT- and [¹¹C] raclopride-PET. All GBA mutation carriers displayed a significant CMRGlc decrease in the supplemental motor area (SMA). The carriers with parkinsonism showed additional hypometabolism in the parietooccipital cortices. The CFT and raclopride PET images in the asymptomatic carriers demonstrated the CFT binding to be within normal values in the putamen and a significant increase was observed in the caudate nucleus while raclopride binding in the striatum was in the normal range. An advanced parkinsonian carrier showed decreased CFT binding and increased raclopride binding in the striatum. The decreased CMRGlc in the SMA was characteristic of the GBA mutation carriers. The hypometabolism in the SMA may, therefore, be involved in the clinical characteristics of parkinsonism associated with GBA mutations when the carriers manifest parkinsonism.
C02	`01`	`X`		`@0 002B17`
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C03	`01`	`X`	`ENG`	`@0 Parkinsonism @2 NM @5 01`
C03	`01`	`X`	`SPA`	`@0 Parkinson síndrome @2 NM @5 01`
C03	`02`	`X`	`FRE`	`@0 Maladie de Parkinson @2 NM @5 02`
C03	`02`	`X`	`ENG`	`@0 Parkinson disease @2 NM @5 02`
C03	`02`	`X`	`SPA`	`@0 Parkinson enfermedad @2 NM @5 02`
C03	`03`	`X`	`FRE`	`@0 Pathologie du système nerveux @5 03`
C03	`03`	`X`	`ENG`	`@0 Nervous system diseases @5 03`
C03	`03`	`X`	`SPA`	`@0 Sistema nervioso patología @5 03`
C03	`04`	`X`	`FRE`	`@0 Imagerie fonctionnelle @5 09`
C03	`04`	`X`	`ENG`	`@0 Functional imaging @5 09`
C03	`04`	`X`	`SPA`	`@0 Imaginería funcional @5 09`
C03	`05`	`X`	`FRE`	`@0 Encéphale @5 10`
C03	`05`	`X`	`ENG`	`@0 Encephalon @5 10`
C03	`05`	`X`	`SPA`	`@0 Encéfalo @5 10`
C03	`06`	`X`	`FRE`	`@0 Mutation @5 11`
C03	`06`	`X`	`ENG`	`@0 Mutation @5 11`
C03	`06`	`X`	`SPA`	`@0 Mutación @5 11`
C03	`07`	`X`	`FRE`	`@0 Porteur @5 12`
C03	`07`	`X`	`ENG`	`@0 Carrier @5 12`
C03	`07`	`X`	`SPA`	`@0 Portador @5 12`
C03	`08`	`X`	`FRE`	`@0 Tomoscintigraphie @5 13`
C03	`08`	`X`	`ENG`	`@0 Emission tomography @5 13`
C03	`08`	`X`	`SPA`	`@0 Tomocentelleografía @5 13`
C03	`09`	`X`	`FRE`	`@0 Tomographie par émission de positons @5 14`
C03	`09`	`X`	`ENG`	`@0 Positron emission tomography @5 14`
C03	`09`	`X`	`SPA`	`@0 Tomografía emisión positrones @5 14`
C03	`10`	`X`	`FRE`	`@0 Glucose(2-désoxy-2-fluor) @2 NK @5 15`
C03	`10`	`X`	`ENG`	`@0 2-deoxy-2-fluoroglucose @2 NK @5 15`
C03	`10`	`X`	`SPA`	`@0 Glucosa(2-desoxi-2-fluoro) @2 NK @5 15`
C03	`11`	`X`	`FRE`	`@0 Raclopride @2 NK @2 FR @5 16`
C03	`11`	`X`	`ENG`	`@0 Raclopride @2 NK @2 FR @5 16`
C03	`11`	`X`	`SPA`	`@0 Racloprida @2 NK @2 FR @5 16`
C07	`01`	`X`	`FRE`	`@0 Système nerveux central @5 37`
C07	`01`	`X`	`ENG`	`@0 Central nervous system @5 37`
C07	`01`	`X`	`SPA`	`@0 Sistema nervioso central @5 37`
C07	`02`	`X`	`FRE`	`@0 Pathologie de l'encéphale @5 39`
C07	`02`	`X`	`ENG`	`@0 Cerebral disorder @5 39`
C07	`02`	`X`	`SPA`	`@0 Encéfalo patología @5 39`
C07	`03`	`X`	`FRE`	`@0 Syndrome extrapyramidal @5 40`
C07	`03`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 40`
C07	`03`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 40`
C07	`04`	`X`	`FRE`	`@0 Maladie dégénérative @5 41`
C07	`04`	`X`	`ENG`	`@0 Degenerative disease @5 41`
C07	`04`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 41`
C07	`05`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 42`
C07	`05`	`X`	`ENG`	`@0 Central nervous system disease @5 42`
C07	`05`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 42`
N21				`@1 291`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

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Le document en format XML

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<author><name sortKey="Kono, Satoshi" sort="Kono, Satoshi" uniqKey="Kono S" first="Satoshi" last="Kono">Satoshi Kono</name>
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<author><name sortKey="Terada, Tatsuhiro" sort="Terada, Tatsuhiro" uniqKey="Terada T" first="Tatsuhiro" last="Terada">Tatsuhiro Terada</name>
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<author><name sortKey="Suzuki, Makiko" sort="Suzuki, Makiko" uniqKey="Suzuki M" first="Makiko" last="Suzuki">Makiko Suzuki</name>
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<author><name sortKey="Miyajima, Hiroaki" sort="Miyajima, Hiroaki" uniqKey="Miyajima H" first="Hiroaki" last="Miyajima">Hiroaki Miyajima</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism</title>
<author><name sortKey="Kono, Satoshi" sort="Kono, Satoshi" uniqKey="Kono S" first="Satoshi" last="Kono">Satoshi Kono</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medicine, Hamamatsu University School of Medicine</s1>
<s2>Hamamatsu</s2>
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<author><name sortKey="Ouchi, Yasuomi" sort="Ouchi, Yasuomi" uniqKey="Ouchi Y" first="Yasuomi" last="Ouchi">Yasuomi Ouchi</name>
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<s3>JPN</s3>
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<author><name sortKey="Terada, Tatsuhiro" sort="Terada, Tatsuhiro" uniqKey="Terada T" first="Tatsuhiro" last="Terada">Tatsuhiro Terada</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medicine, Hamamatsu University School of Medicine</s1>
<s2>Hamamatsu</s2>
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<sZ>3 aut.</sZ>
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<author><name sortKey="Ida, Hiroyuki" sort="Ida, Hiroyuki" uniqKey="Ida H" first="Hiroyuki" last="Ida">Hiroyuki Ida</name>
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<author><name sortKey="Suzuki, Makiko" sort="Suzuki, Makiko" uniqKey="Suzuki M" first="Makiko" last="Suzuki">Makiko Suzuki</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medicine, Hamamatsu University School of Medicine</s1>
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<sZ>1 aut.</sZ>
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<sZ>6 aut.</sZ>
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<author><name sortKey="Miyajima, Hiroaki" sort="Miyajima, Hiroaki" uniqKey="Miyajima H" first="Hiroaki" last="Miyajima">Hiroaki Miyajima</name>
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<sZ>3 aut.</sZ>
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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="2010">2010</date>
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<seriesStmt><title level="j" type="main">Movement disorders</title>
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</seriesStmt>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>2-deoxy-2-fluoroglucose</term>
<term>Carrier</term>
<term>Emission tomography</term>
<term>Encephalon</term>
<term>Functional imaging</term>
<term>Mutation</term>
<term>Nervous system diseases</term>
<term>Parkinson disease</term>
<term>Parkinsonism</term>
<term>Positron emission tomography</term>
<term>Raclopride</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Parkinsonisme</term>
<term>Maladie de Parkinson</term>
<term>Pathologie du   système nerveux</term>
<term>Imagerie fonctionnelle</term>
<term>Encéphale</term>
<term>Mutation</term>
<term>Porteur</term>
<term>Tomoscintigraphie</term>
<term>Tomographie par émission de positons</term>
<term>Glucose(2-désoxy-2-fluor)</term>
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<front><div type="abstract" xml:lang="en">Mutations in the glucocerebrosidase gene (GBA) increase the risk for Parkinson's disease and are also associated with an earlier onset of the disease and an akinetic parkinsonian phenotype. To investigate the underlying pathogenesis of this condition, we assessed cerebral metabolism using positron emission tomography (PET) in GBA mutation carriers with and without parkinsonism. [<sup>18</sup>
F]-fluorodeoxyglucose (FDG)-PET using a three-dimensional stereotactic surface projection analysis was used to measure the cerebral metabolic rates of glucose (CMRGlc) in a patient with parkinsonism and Gaucher disease (GD) and five subjects with a heterozygous GBA mutation, including three patients with parkinsonism and three asymptomatic carriers in comparison to 10 healthy controls in the same age range. Dopaminergic neuronal activity was investigated using [<sup>11</sup>
C] CFT- and [<sup>11</sup>
C] raclopride-PET. All GBA mutation carriers displayed a significant CMRGlc decrease in the supplemental motor area (SMA). The carriers with parkinsonism showed additional hypometabolism in the parietooccipital cortices. The CFT and raclopride PET images in the asymptomatic carriers demonstrated the CFT binding to be within normal values in the putamen and a significant increase was observed in the caudate nucleus while raclopride binding in the striatum was in the normal range. An advanced parkinsonian carrier showed decreased CFT binding and increased raclopride binding in the striatum. The decreased CMRGlc in the SMA was characteristic of the GBA mutation carriers. The hypometabolism in the SMA may, therefore, be involved in the clinical characteristics of parkinsonism associated with GBA mutations when the carriers manifest parkinsonism.</div>
</front>
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<fA11 i1="01" i2="1"><s1>KONO (Satoshi)</s1>
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<fA14 i1="01"><s1>Department of Medicine, Hamamatsu University School of Medicine</s1>
<s2>Hamamatsu</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Laboratory of Human Brain Imaging Research, Molecular Imaging Frontier Research Center, Hamamatsu University School of Medicine</s1>
<s2>Hamamatsu</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Pediatrics, Jikei University School of Medicine</s1>
<s2>Tokyo</s2>
<s3>JPN</s3>
<sZ>4 aut.</sZ>
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<fC01 i1="01" l="ENG"><s0>Mutations in the glucocerebrosidase gene (GBA) increase the risk for Parkinson's disease and are also associated with an earlier onset of the disease and an akinetic parkinsonian phenotype. To investigate the underlying pathogenesis of this condition, we assessed cerebral metabolism using positron emission tomography (PET) in GBA mutation carriers with and without parkinsonism. [<sup>18</sup>
F]-fluorodeoxyglucose (FDG)-PET using a three-dimensional stereotactic surface projection analysis was used to measure the cerebral metabolic rates of glucose (CMRGlc) in a patient with parkinsonism and Gaucher disease (GD) and five subjects with a heterozygous GBA mutation, including three patients with parkinsonism and three asymptomatic carriers in comparison to 10 healthy controls in the same age range. Dopaminergic neuronal activity was investigated using [<sup>11</sup>
C] CFT- and [<sup>11</sup>
C] raclopride-PET. All GBA mutation carriers displayed a significant CMRGlc decrease in the supplemental motor area (SMA). The carriers with parkinsonism showed additional hypometabolism in the parietooccipital cortices. The CFT and raclopride PET images in the asymptomatic carriers demonstrated the CFT binding to be within normal values in the putamen and a significant increase was observed in the caudate nucleus while raclopride binding in the striatum was in the normal range. An advanced parkinsonian carrier showed decreased CFT binding and increased raclopride binding in the striatum. The decreased CMRGlc in the SMA was characteristic of the GBA mutation carriers. The hypometabolism in the SMA may, therefore, be involved in the clinical characteristics of parkinsonism associated with GBA mutations when the carriers manifest parkinsonism.</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>Parkinsonisme</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Parkinsonism</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Parkinson síndrome</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Pathologie du   système nerveux</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Imagerie fonctionnelle</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Functional imaging</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Imaginería funcional</s0>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Encephalon</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>10</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Mutation</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Mutation</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Mutación</s0>
<s5>11</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Porteur</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Carrier</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Portador</s0>
<s5>12</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Tomoscintigraphie</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Emission tomography</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Tomocentelleografía</s0>
<s5>13</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Tomographie par émission de positons</s0>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Positron emission tomography</s0>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Tomografía emisión positrones</s0>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Glucose(2-désoxy-2-fluor)</s0>
<s2>NK</s2>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>2-deoxy-2-fluoroglucose</s0>
<s2>NK</s2>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Glucosa(2-desoxi-2-fluoro)</s0>
<s2>NK</s2>
<s5>15</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Raclopride</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>16</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Raclopride</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>16</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Racloprida</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>16</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>39</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>40</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du   système nerveux central</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>42</s5>
</fC07>
<fN21><s1>291</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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	Movement Disorders (revue)
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Movement Disorders (revue)

Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism

Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism

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