PET Study of Brain Acetylcholinesterase in Cerebellar Degenerative Disorders
Identifieur interne : 001B02 ( PascalFrancis/Curation ); précédent : 001B01; suivant : 001B03PET Study of Brain Acetylcholinesterase in Cerebellar Degenerative Disorders
Auteurs : Shigeki Hirano [Japon] ; Hitoshi Shinotoh [Japon] ; Kimihito Arai [Japon] ; Akiyo Aotsuka [Japon] ; Fumihiko Yasuno [Japon] ; Noriko Tanaka [Japon] ; Tsuneyoshi Ota [Japon] ; Koichi Sato [Japon] ; Kiyoshi Fukushi [Japon] ; Shuji Tanada [Japon] ; Takamichi Hattori [Japon] ; Toshiaki Irie [Japon]Source :
- Movement disorders [ 0885-3185 ] ; 2008.
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- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
To elucidate characteristic changes of brain acetylcholinesterase (AChE) in cerebellar degenerative disorders. Eight patients with the cerebellar variant of multiple system atrophy (MSA-C), 7 patients with spinocerebellar ataxia type-3 (SCA-3), 3 patients with SCA-6, and 13 healthy age-matched volunteers participated in this study. Brain AChE activity was measured by ["C] N-methylpiperidin-4-yl propionate PET in all subjects. Brain AChE activities were significantly decreased in the thalamus (-27%) and the posterior lobe of cerebellar cortex (-36%) in patients with MSA-C and in the thalamus (-23%) in patients with SCA-3 compared with healthy controls (P < 0.01). Thalamic AChE activities of SCA-3 patients were negatively correlated with the unified Parkinson's disease rating scale motor subscore (P < 0.001). AChE activities were not significantly altered in the cerebral cortex in any disease group. Reduction of AChE activities in the thalamus and cerebellum in MSA and in the thalamus in SCA-3 suggest that cholinergic modulating drugs may have a role in the treatment of ataxia and other symptoms in these disorders.
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">PET Study of Brain Acetylcholinesterase in Cerebellar Degenerative Disorders</title>
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<author><name sortKey="Arai, Kimihito" sort="Arai, Kimihito" uniqKey="Arai K" first="Kimihito" last="Arai">Kimihito Arai</name>
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<author><name sortKey="Aotsuka, Akiyo" sort="Aotsuka, Akiyo" uniqKey="Aotsuka A" first="Akiyo" last="Aotsuka">Akiyo Aotsuka</name>
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<author><name sortKey="Yasuno, Fumihiko" sort="Yasuno, Fumihiko" uniqKey="Yasuno F" first="Fumihiko" last="Yasuno">Fumihiko Yasuno</name>
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<author><name sortKey="Tanaka, Noriko" sort="Tanaka, Noriko" uniqKey="Tanaka N" first="Noriko" last="Tanaka">Noriko Tanaka</name>
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<author><name sortKey="Ota, Tsuneyoshi" sort="Ota, Tsuneyoshi" uniqKey="Ota T" first="Tsuneyoshi" last="Ota">Tsuneyoshi Ota</name>
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<author><name sortKey="Sato, Koichi" sort="Sato, Koichi" uniqKey="Sato K" first="Koichi" last="Sato">Koichi Sato</name>
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<author><name sortKey="Fukushi, Kiyoshi" sort="Fukushi, Kiyoshi" uniqKey="Fukushi K" first="Kiyoshi" last="Fukushi">Kiyoshi Fukushi</name>
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<term>Multiple system atrophy</term>
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<term>Tomographie par émission de positons</term>
<term>Encéphale</term>
<term>Acetylcholinesterase</term>
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<front><div type="abstract" xml:lang="en">To elucidate characteristic changes of brain acetylcholinesterase (AChE) in cerebellar degenerative disorders. Eight patients with the cerebellar variant of multiple system atrophy (MSA-C), 7 patients with spinocerebellar ataxia type-3 (SCA-3), 3 patients with SCA-6, and 13 healthy age-matched volunteers participated in this study. Brain AChE activity was measured by ["C] N-methylpiperidin-4-yl propionate PET in all subjects. Brain AChE activities were significantly decreased in the thalamus (-27%) and the posterior lobe of cerebellar cortex (-36%) in patients with MSA-C and in the thalamus (-23%) in patients with SCA-3 compared with healthy controls (P < 0.01). Thalamic AChE activities of SCA-3 patients were negatively correlated with the unified Parkinson's disease rating scale motor subscore (P < 0.001). AChE activities were not significantly altered in the cerebral cortex in any disease group. Reduction of AChE activities in the thalamus and cerebellum in MSA and in the thalamus in SCA-3 suggest that cholinergic modulating drugs may have a role in the treatment of ataxia and other symptoms in these disorders.</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>23</s2>
</fA05>
<fA06><s2>8</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>PET Study of Brain Acetylcholinesterase in Cerebellar Degenerative Disorders</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>HIRANO (Shigeki)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>SHINOTOH (Hitoshi)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>ARAI (Kimihito)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>AOTSUKA (Akiyo)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>YASUNO (Fumihiko)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>TANAKA (Noriko)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>OTA (Tsuneyoshi)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>SATO (Koichi)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>FUKUSHI (Kiyoshi)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>TANADA (Shuji)</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>HATTORI (Takamichi)</s1>
</fA11>
<fA11 i1="12" i2="1"><s1>IRIE (Toshiaki)</s1>
</fA11>
<fA14 i1="01"><s1>epartment of Neurology, Chiba University Graduate School of Medicine</s1>
<s2>Chiba</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>11 aut.</sZ>
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<fA14 i1="02"><s1>Molecular Probe Group, Molecular Imaging Center, National Institute of Radiological Sciences</s1>
<s2>Chiba</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Asahi Hospital for Neurological Diseases</s1>
<s2>Chiba</s2>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Neurology, National Hospital Organization Chiba-East Hospital</s1>
<s2>Chiba</s2>
<s3>JPN</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Neurology, Chiba Aoba Municipal Hospital</s1>
<s2>Chiba</s2>
<s3>JPN</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Department of Psychiatry, University of Tsukuba Hospital</s1>
<s2>Ibaraki</s2>
<s3>JPN</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Department of Neurosurgery, Tokyo Women's Medical University, Medical Center East</s1>
<s2>Tokyo</s2>
<s3>JPN</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Department of Psychiatry, Juntendo University School of Medicine</s1>
<s2>Tokyo</s2>
<s3>JPN</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="09"><s1>Department of Psychiatry, Teikyo University School of Medicine, Ichihara Hospital</s1>
<s2>Chiba</s2>
<s3>JPN</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="10"><s1>National Institute of Radiological Sciences</s1>
<s2>Chiba</s2>
<s3>JPN</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA20><s1>1154-1160</s1>
</fA20>
<fA21><s1>2008</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000196042800120</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2008 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>31 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>08-0357257</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>To elucidate characteristic changes of brain acetylcholinesterase (AChE) in cerebellar degenerative disorders. Eight patients with the cerebellar variant of multiple system atrophy (MSA-C), 7 patients with spinocerebellar ataxia type-3 (SCA-3), 3 patients with SCA-6, and 13 healthy age-matched volunteers participated in this study. Brain AChE activity was measured by ["C] N-methylpiperidin-4-yl propionate PET in all subjects. Brain AChE activities were significantly decreased in the thalamus (-27%) and the posterior lobe of cerebellar cortex (-36%) in patients with MSA-C and in the thalamus (-23%) in patients with SCA-3 compared with healthy controls (P < 0.01). Thalamic AChE activities of SCA-3 patients were negatively correlated with the unified Parkinson's disease rating scale motor subscore (P < 0.001). AChE activities were not significantly altered in the cerebral cortex in any disease group. Reduction of AChE activities in the thalamus and cerebellum in MSA and in the thalamus in SCA-3 suggest that cholinergic modulating drugs may have a role in the treatment of ataxia and other symptoms in these disorders.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B24B07</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Atrophie multisystématisée</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Multiple system atrophy</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Atrofia multisistematizada</s0>
<s2>NM</s2>
<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>Tomoscintigraphie</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Emission tomography</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Tomocentelleografía</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Tomographie par émission de positons</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Positron emission tomography</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Tomografía emisión positrones</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Encephalon</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Acetylcholinesterase</s0>
<s2>FE</s2>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Acetylcholinesterase</s0>
<s2>FE</s2>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Acetylcholinesterase</s0>
<s2>FE</s2>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Cervelet</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Cerebellum</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Cerebelo</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Ataxie spinocérébelleuse</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Spinocerebellar ataxia</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Ataxia spinocerebelosa</s0>
<s2>NM</s2>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Acétylcholine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Acetylcholine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Acetilcolina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Thalamus</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Thalamus</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Tálamo</s0>
<s5>16</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Carboxylic ester hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Carboxylic ester hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Carboxylic ester hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Esterases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Esterases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Esterases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Maladie héréditaire</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Genetic disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>42</s5>
</fC07>
<fN21><s1>224</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>
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