Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism
Identifieur interne : 000935 ( PascalFrancis/Corpus ); précédent : 000934; suivant : 000936Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism
Auteurs : Satoshi Kono ; Yasuomi Ouchi ; Tatsuhiro Terada ; Hiroyuki Ida ; Makiko Suzuki ; Hiroaki MiyajimaSource :
- Movement disorders [ 0885-3185 ] ; 2010.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
pA |
|
---|
Format Inist (serveur)
NO : | PASCAL 10-0446278 INIST |
---|---|
ET : | Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism |
AU : | KONO (Satoshi); OUCHI (Yasuomi); TERADA (Tatsuhiro); IDA (Hiroyuki); SUZUKI (Makiko); MIYAJIMA (Hiroaki) |
AF : | Department of Medicine, Hamamatsu University School of Medicine/Hamamatsu/Japon (1 aut., 3 aut., 5 aut., 6 aut.); Laboratory of Human Brain Imaging Research, Molecular Imaging Frontier Research Center, Hamamatsu University School of Medicine/Hamamatsu/Japon (2 aut.); Department of Pediatrics, Jikei University School of Medicine/Tokyo/Japon (4 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2010; Vol. 25; No. 12; Pp. 1823-1829; Bibl. 35 ref. |
LA : | Anglais |
EA : | 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. |
CC : | 002B17; 002B17G |
FD : | 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 |
FG : | Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central |
ED : | Parkinsonism; Parkinson disease; Nervous system diseases; Functional imaging; Encephalon; Mutation; Carrier; Emission tomography; Positron emission tomography; 2-deoxy-2-fluoroglucose; Raclopride |
EG : | Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease |
SD : | Parkinson síndrome; Parkinson enfermedad; Sistema nervioso patología; Imaginería funcional; Encéfalo; Mutación; Portador; Tomocentelleografía; Tomografía emisión positrones; Glucosa(2-desoxi-2-fluoro); Racloprida |
LO : | INIST-20953.354000194841700070 |
ID : | 10-0446278 |
Links to Exploration step
Pascal:10-0446278Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><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><inist: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>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ouchi, Yasuomi" sort="Ouchi, Yasuomi" uniqKey="Ouchi Y" first="Yasuomi" last="Ouchi">Yasuomi Ouchi</name>
<affiliation><inist: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>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Terada, Tatsuhiro" sort="Terada, Tatsuhiro" uniqKey="Terada T" first="Tatsuhiro" last="Terada">Tatsuhiro Terada</name>
<affiliation><inist: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>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ida, Hiroyuki" sort="Ida, Hiroyuki" uniqKey="Ida H" first="Hiroyuki" last="Ida">Hiroyuki Ida</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Pediatrics, Jikei University School of Medicine</s1>
<s2>Tokyo</s2>
<s3>JPN</s3>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Suzuki, Makiko" sort="Suzuki, Makiko" uniqKey="Suzuki M" first="Makiko" last="Suzuki">Makiko Suzuki</name>
<affiliation><inist: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>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Miyajima, Hiroaki" sort="Miyajima, Hiroaki" uniqKey="Miyajima H" first="Hiroaki" last="Miyajima">Hiroaki Miyajima</name>
<affiliation><inist: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>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">10-0446278</idno>
<date when="2010">2010</date>
<idno type="stanalyst">PASCAL 10-0446278 INIST</idno>
<idno type="RBID">Pascal:10-0446278</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000935</idno>
</publicationStmt>
<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><inist: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>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ouchi, Yasuomi" sort="Ouchi, Yasuomi" uniqKey="Ouchi Y" first="Yasuomi" last="Ouchi">Yasuomi Ouchi</name>
<affiliation><inist: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>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Terada, Tatsuhiro" sort="Terada, Tatsuhiro" uniqKey="Terada T" first="Tatsuhiro" last="Terada">Tatsuhiro Terada</name>
<affiliation><inist: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>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Ida, Hiroyuki" sort="Ida, Hiroyuki" uniqKey="Ida H" first="Hiroyuki" last="Ida">Hiroyuki Ida</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Pediatrics, Jikei University School of Medicine</s1>
<s2>Tokyo</s2>
<s3>JPN</s3>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Suzuki, Makiko" sort="Suzuki, Makiko" uniqKey="Suzuki M" first="Makiko" last="Suzuki">Makiko Suzuki</name>
<affiliation><inist: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>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Miyajima, Hiroaki" sort="Miyajima, Hiroaki" uniqKey="Miyajima H" first="Hiroaki" last="Miyajima">Hiroaki Miyajima</name>
<affiliation><inist: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>
</inist:fA14>
</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="2010">2010</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>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>
<term>Raclopride</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<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>
</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>25</s2>
</fA05>
<fA06><s2>12</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>KONO (Satoshi)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>OUCHI (Yasuomi)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>TERADA (Tatsuhiro)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>IDA (Hiroyuki)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>SUZUKI (Makiko)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>MIYAJIMA (Hiroaki)</s1>
</fA11>
<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>
</fA14>
<fA20><s1>1823-1829</s1>
</fA20>
<fA21><s1>2010</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000194841700070</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2010 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>35 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>10-0446278</s0>
</fA47>
<fA60><s1>P</s1>
</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>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>
<server><NO>PASCAL 10-0446278 INIST</NO>
<ET>Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism</ET>
<AU>KONO (Satoshi); OUCHI (Yasuomi); TERADA (Tatsuhiro); IDA (Hiroyuki); SUZUKI (Makiko); MIYAJIMA (Hiroaki)</AU>
<AF>Department of Medicine, Hamamatsu University School of Medicine/Hamamatsu/Japon (1 aut., 3 aut., 5 aut., 6 aut.); Laboratory of Human Brain Imaging Research, Molecular Imaging Frontier Research Center, Hamamatsu University School of Medicine/Hamamatsu/Japon (2 aut.); Department of Pediatrics, Jikei University School of Medicine/Tokyo/Japon (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2010; Vol. 25; No. 12; Pp. 1823-1829; Bibl. 35 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B17; 002B17G</CC>
<FD>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</FD>
<FG>Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central</FG>
<ED>Parkinsonism; Parkinson disease; Nervous system diseases; Functional imaging; Encephalon; Mutation; Carrier; Emission tomography; Positron emission tomography; 2-deoxy-2-fluoroglucose; Raclopride</ED>
<EG>Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG>
<SD>Parkinson síndrome; Parkinson enfermedad; Sistema nervioso patología; Imaginería funcional; Encéfalo; Mutación; Portador; Tomocentelleografía; Tomografía emisión positrones; Glucosa(2-desoxi-2-fluoro); Racloprida</SD>
<LO>INIST-20953.354000194841700070</LO>
<ID>10-0446278</ID>
</server>
</inist>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PascalFrancis/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000935 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 000935 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Santé |area= MovDisordV3 |flux= PascalFrancis |étape= Corpus |type= RBID |clé= Pascal:10-0446278 |texte= Functional Brain Imaging in Glucocerebrosidase Mutation Carriers With and Without Parkinsonism }}
This area was generated with Dilib version V0.6.23. |