Studies on neurotransmitter markers of the basal ganglia in Pick's disease, with special reference to dopamine reduction
Identifieur interne : 002E51 ( Main/Corpus ); précédent : 002E50; suivant : 002E52Studies on neurotransmitter markers of the basal ganglia in Pick's disease, with special reference to dopamine reduction
Auteurs : Ichiro Kanazawa ; Shin Kwak ; Hidenao Sasaki ; Osamu Muramoto ; Toshio Mizutani ; Akira Hori ; Nobuyuki NukinaSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1987.
Abstract
γ-Aminobutyric acid (GABA), substance P and dopamine concentrations and choline acetyltransferase (ChAT) activity were measured in post-mortem cerebro-cortical and basal ganglial areas of 14 controls and 4 patients with pathologically verified Pick's disease (1 classic case and 3 cases of the generalized form). GABA and substance P levels in the substantia nigra and the globus pallidus were generally decreased, corresponding to the moderate to severe loss of small neurones in the striatum. ChAT activities in the striatum varied from case to case, in proportion to various degrees of loss of large neurones in the striatum. These neurotransmitter abnormalities in Pick's disease were exactly the same as those in Huntington's disease. However, dopamine concentrations were markedly reduced in the striatum in Pick's disease, whereas striatal dopamine in Huntington's disease is reported to be increased. A dopamine reduction in the striatum of Pick's disease was more disproportionately prominent than expected for various degrees of nigral cell loss. This may be one of the important factors which prevents the generation of choreic movements in Pick's disease in spite of definite striatal atrophy similar to Huntington's disease.
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DOI: 10.1016/0022-510X(88)90020-2
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Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation></affiliation></author><author><name sortKey="Muramoto, Osamu" sort="Muramoto, Osamu" uniqKey="Muramoto O" first="Osamu" last="Muramoto">Osamu Muramoto</name><affiliation><mods:affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation></affiliation></author><author><name sortKey="Mizutani, Toshio" sort="Mizutani, Toshio" uniqKey="Mizutani T" first="Toshio" last="Mizutani">Toshio Mizutani</name><affiliation><mods:affiliation>Division of Clinical Neuropathology, Metropolitan Institute of Neurological Research, Tokyo 118 Japan</mods:affiliation></affiliation></author><author><name sortKey="Hori, Akira" sort="Hori, Akira" uniqKey="Hori A" first="Akira" last="Hori">Akira Hori</name><affiliation><mods:affiliation>Department of Pathology, University of Göttingen, Göttingen F.R.G.</mods:affiliation></affiliation></author><author><name sortKey="Nukina, Nobuyuki" sort="Nukina, Nobuyuki" uniqKey="Nukina N" first="Nobuyuki" last="Nukina">Nobuyuki Nukina</name><affiliation><mods:affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:60F8C350DF5B61978A2C138D6BBF993EF15F084C</idno><date when="1988" year="1988">1988</date><idno type="doi">10.1016/0022-510X(88)90020-2</idno><idno type="url">https://api.istex.fr/document/60F8C350DF5B61978A2C138D6BBF993EF15F084C/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002E51</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Studies on neurotransmitter markers of the basal ganglia in Pick's disease, with special reference to dopamine reduction</title><author><name sortKey="Kanazawa, Ichiro" sort="Kanazawa, Ichiro" 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Muramoto</name><affiliation><mods:affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</mods:affiliation></affiliation></author><author><name sortKey="Mizutani, Toshio" sort="Mizutani, Toshio" uniqKey="Mizutani T" first="Toshio" last="Mizutani">Toshio Mizutani</name><affiliation><mods:affiliation>Division of Clinical Neuropathology, Metropolitan Institute of Neurological Research, Tokyo 118 Japan</mods:affiliation></affiliation></author><author><name sortKey="Hori, Akira" sort="Hori, Akira" uniqKey="Hori A" first="Akira" last="Hori">Akira Hori</name><affiliation><mods:affiliation>Department of Pathology, University of Göttingen, Göttingen F.R.G.</mods:affiliation></affiliation></author><author><name sortKey="Nukina, Nobuyuki" sort="Nukina, Nobuyuki" uniqKey="Nukina N" first="Nobuyuki" last="Nukina">Nobuyuki Nukina</name><affiliation><mods:affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="ISSN">0022-510X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1987">1987</date><biblScope unit="volume">83</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="63">63</biblScope><biblScope unit="page" to="74">74</biblScope></imprint><idno type="ISSN">0022-510X</idno></series><idno type="istex">60F8C350DF5B61978A2C138D6BBF993EF15F084C</idno><idno type="DOI">10.1016/0022-510X(88)90020-2</idno><idno type="PII">0022-510X(88)90020-2</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-510X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">γ-Aminobutyric acid (GABA), substance P and dopamine concentrations and choline acetyltransferase (ChAT) activity were measured in post-mortem cerebro-cortical and basal ganglial areas of 14 controls and 4 patients with pathologically verified Pick's disease (1 classic case and 3 cases of the generalized form). GABA and substance P levels in the substantia nigra and the globus pallidus were generally decreased, corresponding to the moderate to severe loss of small neurones in the striatum. ChAT activities in the striatum varied from case to case, in proportion to various degrees of loss of large neurones in the striatum. These neurotransmitter abnormalities in Pick's disease were exactly the same as those in Huntington's disease. However, dopamine concentrations were markedly reduced in the striatum in Pick's disease, whereas striatal dopamine in Huntington's disease is reported to be increased. A dopamine reduction in the striatum of Pick's disease was more disproportionately prominent than expected for various degrees of nigral cell loss. This may be one of the important factors which prevents the generation of choreic movements in Pick's disease in spite of definite striatal atrophy similar to Huntington's disease.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Ichiro Kanazawa</name><affiliations><json:string>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</json:string></affiliations></json:item><json:item><name>Shin Kwak</name><affiliations><json:string>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</json:string></affiliations></json:item><json:item><name>Hidenao Sasaki</name><affiliations><json:string>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</json:string></affiliations></json:item><json:item><name>Osamu Muramoto</name><affiliations><json:string>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</json:string></affiliations></json:item><json:item><name>Toshio Mizutani</name><affiliations><json:string>Division of Clinical Neuropathology, Metropolitan Institute of Neurological Research, Tokyo 118 Japan</json:string></affiliations></json:item><json:item><name>Akira Hori</name><affiliations><json:string>Department of Pathology, University of Göttingen, Göttingen F.R.G.</json:string></affiliations></json:item><json:item><name>Nobuyuki Nukina</name><affiliations><json:string>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Pick's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>GABA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Substance P</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Choline acetyltransferase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Basal ganglia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Chorea</value></json:item></subject><language><json:string>eng</json:string></language><abstract>γ-Aminobutyric acid (GABA), substance P and dopamine concentrations and choline acetyltransferase (ChAT) activity were measured in post-mortem cerebro-cortical and basal ganglial areas of 14 controls and 4 patients with pathologically verified Pick's disease (1 classic case and 3 cases of the generalized form). GABA and substance P levels in the substantia nigra and the globus pallidus were generally decreased, corresponding to the moderate to severe loss of small neurones in the striatum. ChAT activities in the striatum varied from case to case, in proportion to various degrees of loss of large neurones in the striatum. These neurotransmitter abnormalities in Pick's disease were exactly the same as those in Huntington's disease. However, dopamine concentrations were markedly reduced in the striatum in Pick's disease, whereas striatal dopamine in Huntington's disease is reported to be increased. A dopamine reduction in the striatum of Pick's disease was more disproportionately prominent than expected for various degrees of nigral cell loss. This may be one of the important factors which prevents the generation of choreic movements in Pick's disease in spite of definite striatal atrophy similar to Huntington's disease.</abstract><qualityIndicators><score>7.231</score><pdfVersion>1.4</pdfVersion><pdfPageSize>504 x 720 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1237</abstractCharCount><pdfWordCount>4535</pdfWordCount><pdfCharCount>27097</pdfCharCount><pdfPageCount>12</pdfPageCount><abstractWordCount>183</abstractWordCount></qualityIndicators><title>Studies on neurotransmitter markers of the basal ganglia in Pick's disease, with special reference to dopamine reduction</title><pii><json:string>0022-510X(88)90020-2</json:string></pii><genre><json:string>research-article</json:string></genre><serie><pages><last>378</last><first>298</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Handbook of Clinical Neurology, Vol. 6 (Disease of 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Ibaraki-ken 305 Japan</affiliation></author><author><persName><forename type="first">Shin</forename><surname>Kwak</surname></persName><affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</affiliation></author><author><persName><forename type="first">Hidenao</forename><surname>Sasaki</surname></persName><note type="biography">Present address: Division of Neurology, Hokuyukai Neurological Hospital, Sapporo 064, Japan.</note><affiliation>Present address: Division of Neurology, Hokuyukai Neurological Hospital, Sapporo 064, Japan.</affiliation><affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</affiliation></author><author><persName><forename type="first">Osamu</forename><surname>Muramoto</surname></persName><affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</affiliation></author><author><persName><forename type="first">Toshio</forename><surname>Mizutani</surname></persName><affiliation>Division of Clinical Neuropathology, Metropolitan Institute of Neurological Research, Tokyo 118 Japan</affiliation></author><author><persName><forename type="first">Akira</forename><surname>Hori</surname></persName><affiliation>Department of Pathology, University of Göttingen, Göttingen F.R.G.</affiliation></author><author><persName><forename type="first">Nobuyuki</forename><surname>Nukina</surname></persName><affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</affiliation></author></analytic><monogr><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="pISSN">0022-510X</idno><idno type="PII">S0022-510X(00)X0273-0</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1987"></date><biblScope unit="volume">83</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="63">63</biblScope><biblScope unit="page" to="74">74</biblScope></imprint></monogr><idno type="istex">60F8C350DF5B61978A2C138D6BBF993EF15F084C</idno><idno type="DOI">10.1016/0022-510X(88)90020-2</idno><idno type="PII">0022-510X(88)90020-2</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1988</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>γ-Aminobutyric acid (GABA), substance P and dopamine concentrations and choline acetyltransferase (ChAT) activity were measured in post-mortem cerebro-cortical and basal ganglial areas of 14 controls and 4 patients with pathologically verified Pick's disease (1 classic case and 3 cases of the generalized form). GABA and substance P levels in the substantia nigra and the globus pallidus were generally decreased, corresponding to the moderate to severe loss of small neurones in the striatum. ChAT activities in the striatum varied from case to case, in proportion to various degrees of loss of large neurones in the striatum. These neurotransmitter abnormalities in Pick's disease were exactly the same as those in Huntington's disease. However, dopamine concentrations were markedly reduced in the striatum in Pick's disease, whereas striatal dopamine in Huntington's disease is reported to be increased. A dopamine reduction in the striatum of Pick's disease was more disproportionately prominent than expected for various degrees of nigral cell loss. This may be one of the important factors which prevents the generation of choreic movements in Pick's disease in spite of definite striatal atrophy similar to Huntington's disease.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Pick's disease</term></item><item><term>GABA</term></item><item><term>Substance P</term></item><item><term>Choline acetyltransferase</term></item><item><term>Dopamine</term></item><item><term>Basal ganglia</term></item><item><term>Chorea</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1987-08-25">Registration</change><change when="1987-08-24">Modified</change><change when="1987">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>JNS</jid><aid>88900202</aid><ce:pii>0022-510X(88)90020-2</ce:pii><ce:doi>10.1016/0022-510X(88)90020-2</ce:doi><ce:copyright type="unknown" year="1988"></ce:copyright></item-info><head><ce:title>Studies on neurotransmitter markers of the basal ganglia in Pick's disease, with special reference to dopamine reduction</ce:title><ce:author-group><ce:author><ce:given-name>Ichiro</ce:given-name><ce:surname>Kanazawa</ce:surname><ce:cross-ref refid="COR1"><ce:sup>1</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Shin</ce:given-name><ce:surname>Kwak</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>2</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Hidenao</ce:given-name><ce:surname>Sasaki</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Osamu</ce:given-name><ce:surname>Muramoto</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Toshio</ce:given-name><ce:surname>Mizutani</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>3</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Akira</ce:given-name><ce:surname>Hori</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>4</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Nobuyuki</ce:given-name><ce:surname>Nukina</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>2</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Division of Clinical Neuropathology, Metropolitan Institute of Neurological Research, Tokyo 118 Japan</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>d</ce:label><ce:textfn>Department of Pathology, University of Göttingen, Göttingen F.R.G.</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>1</ce:label><ce:text>Correspondence to: Ichiro Kanazawa, Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305, Japan.</ce:text></ce:correspondence><ce:footnote id="FN1"><ce:label>∗</ce:label><ce:note-para>Present address: Division of Neurology, Hokuyukai Neurological Hospital, Sapporo 064, Japan.</ce:note-para></ce:footnote></ce:author-group><ce:date-received day="21" month="4" year="1987"></ce:date-received><ce:date-revised day="24" month="8" year="1987"></ce:date-revised><ce:date-accepted day="25" month="8" year="1987"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>γ-Aminobutyric acid (GABA), substance P and dopamine concentrations and choline acetyltransferase (ChAT) activity were measured in post-mortem cerebro-cortical and basal ganglial areas of 14 controls and 4 patients with pathologically verified Pick's disease (1 classic case and 3 cases of the generalized form). GABA and substance P levels in the substantia nigra and the globus pallidus were generally decreased, corresponding to the moderate to severe loss of small neurones in the striatum. ChAT activities in the striatum varied from case to case, in proportion to various degrees of loss of large neurones in the striatum. These neurotransmitter abnormalities in Pick's disease were exactly the same as those in Huntington's disease. However, dopamine concentrations were markedly reduced in the striatum in Pick's disease, whereas striatal dopamine in Huntington's disease is reported to be increased. A dopamine reduction in the striatum of Pick's disease was more disproportionately prominent than expected for various degrees of nigral cell loss. This may be one of the important factors which prevents the generation of choreic movements in Pick's disease in spite of definite striatal atrophy similar to Huntington's disease.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Pick's disease</ce:text></ce:keyword><ce:keyword><ce:text>GABA</ce:text></ce:keyword><ce:keyword><ce:text>Substance P</ce:text></ce:keyword><ce:keyword><ce:text>Choline acetyltransferase</ce:text></ce:keyword><ce:keyword><ce:text>Dopamine</ce:text></ce:keyword><ce:keyword><ce:text>Basal ganglia</ce:text></ce:keyword><ce:keyword><ce:text>Chorea</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Studies on neurotransmitter markers of the basal ganglia in Pick's disease, with special reference to dopamine reduction</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Studies on neurotransmitter markers of the basal ganglia in Pick's disease, with special reference to dopamine reduction</title></titleInfo><name type="personal"><namePart type="given">Ichiro</namePart><namePart type="family">Kanazawa</namePart><affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</affiliation><description>Correspondence to: Ichiro Kanazawa, Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305, Japan.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Shin</namePart><namePart type="family">Kwak</namePart><affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hidenao</namePart><namePart type="family">Sasaki</namePart><affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</affiliation><description>Present address: Division of Neurology, Hokuyukai Neurological Hospital, Sapporo 064, Japan.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Osamu</namePart><namePart type="family">Muramoto</namePart><affiliation>Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, Ibaraki-ken 305 Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Toshio</namePart><namePart type="family">Mizutani</namePart><affiliation>Division of Clinical Neuropathology, Metropolitan Institute of Neurological Research, Tokyo 118 Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Akira</namePart><namePart type="family">Hori</namePart><affiliation>Department of Pathology, University of Göttingen, Göttingen F.R.G.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nobuyuki</namePart><namePart type="family">Nukina</namePart><affiliation>Department of Neurology, Institute of Brain Research, University of Tokyo, Tokyo 113 Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1987</dateIssued><dateValid encoding="w3cdtf">1987-08-25</dateValid><dateModified encoding="w3cdtf">1987-08-24</dateModified><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">γ-Aminobutyric acid (GABA), substance P and dopamine concentrations and choline acetyltransferase (ChAT) activity were measured in post-mortem cerebro-cortical and basal ganglial areas of 14 controls and 4 patients with pathologically verified Pick's disease (1 classic case and 3 cases of the generalized form). GABA and substance P levels in the substantia nigra and the globus pallidus were generally decreased, corresponding to the moderate to severe loss of small neurones in the striatum. ChAT activities in the striatum varied from case to case, in proportion to various degrees of loss of large neurones in the striatum. These neurotransmitter abnormalities in Pick's disease were exactly the same as those in Huntington's disease. However, dopamine concentrations were markedly reduced in the striatum in Pick's disease, whereas striatal dopamine in Huntington's disease is reported to be increased. A dopamine reduction in the striatum of Pick's disease was more disproportionately prominent than expected for various degrees of nigral cell loss. This may be one of the important factors which prevents the generation of choreic movements in Pick's disease in spite of definite striatal atrophy similar to Huntington's disease.</abstract><subject><genre>Keywords</genre><topic>Pick's disease</topic><topic>GABA</topic><topic>Substance P</topic><topic>Choline acetyltransferase</topic><topic>Dopamine</topic><topic>Basal ganglia</topic><topic>Chorea</topic></subject><relatedItem type="host"><titleInfo><title>Journal of the Neurological Sciences</title></titleInfo><titleInfo type="abbreviated"><title>JNS</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">198801</dateIssued></originInfo><identifier type="ISSN">0022-510X</identifier><identifier type="PII">S0022-510X(00)X0273-0</identifier><part><date>198801</date><detail type="volume"><number>83</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>128</end></extent><extent unit="pages"><start>63</start><end>74</end></extent></part></relatedItem><identifier type="istex">60F8C350DF5B61978A2C138D6BBF993EF15F084C</identifier><identifier type="DOI">10.1016/0022-510X(88)90020-2</identifier><identifier type="PII">0022-510X(88)90020-2</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/60F8C350DF5B61978A2C138D6BBF993EF15F084C/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROIMAGING</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments></istex></record>Pour manipuler ce document sous Unix (Dilib)
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