Striatal dihydroxyphenylalanine decarboxylase and tyrosine hydroxylase protein in idiopathic Parkinson's disease and dominantly inherited olivopontocerebellar atrophy
Identifieur interne : 000B05 ( Istex/Corpus ); précédent : 000B04; suivant : 000B06Striatal dihydroxyphenylalanine decarboxylase and tyrosine hydroxylase protein in idiopathic Parkinson's disease and dominantly inherited olivopontocerebellar atrophy
Auteurs : Xiao-Hui Zhong ; John W. Haycock ; Kathleen Shannak ; Yves Robitaille ; Jonathan Fratkin ; Arnuf H. Koeppen ; Oleh Hornykiewicz ; KishSource :
- Movement Disorders [ 0885-3185 ] ; 1995-01.
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- KwdEn :
Abstract
We measured the levels of dopamine, tyrosine hydroxylase (TH) protein, and dihydroxyphenylalanine (DOPA) decarboxylase (DDC) protein in the striatum of 10 patients with idiopathic Parkinson's disease (PD) and 23 patients with dominantly inherited olivopontocerebellar atrophy (OPCA). The levels of dopamine were markedly reduced (2% of control) in the striatum of the patients with PD, whereas striatal dopamine in the patients with OPCA ranged from normal (<60% of control) to moderately reduced (20–60% of control) to severely depleted (<20% of control). Both TH and DDC protein levels were significantly lower than those of the controls in the striatum of all of the patients with PD and in the subgroup of patients with OPCA having severely depleted dopamine. In contradistinction, TH but not DDC protein levels were reduced in those patients with OPCA having moderately reduced dopamine levels. This suggests that in the early stage of nigrostriatal dopamine neurone degeneration, DDC levels may be less susceptible to neurodegenerative influences than is TH synthesis or, alternatively, DDC synthesis may be more aggressively upregulated. Unexpectedly, from the blot immunolabeling analysis an additional DDC‐immunoreactive band of slightly lower apparent molecular mass was detected in two of the patients with PD and in 12 of the patients with OPCA. This additional DDC band, which was not present in any of the control subjects, may reflect posttranslational modification(s) of DDC related to the neurodegenerative process.
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DOI: 10.1002/mds.870100104
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ISTEX:34AD1A9AA121CA42789265D7FF5002FA00623C49Le document en format XML
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Koeppen</name><affiliation><mods:affiliation>Veterans Administration Medical Center, Albany, New York, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Hornykiewicz, Oleh" sort="Hornykiewicz, Oleh" uniqKey="Hornykiewicz O" first="Oleh" last="Hornykiewicz">Oleh Hornykiewicz</name><affiliation><mods:affiliation>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Biochemical Pharmacology, University of Vienna, Vienna, Austria</mods:affiliation></affiliation></author><author><name sortKey="Kish" sort="Kish" uniqKey="Kish" last="Kish">Kish</name><affiliation><mods:affiliation>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-01">1995-01</date><biblScope unit="vol">10</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="10">10</biblScope><biblScope unit="page" to="17">17</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">34AD1A9AA121CA42789265D7FF5002FA00623C49</idno><idno type="DOI">10.1002/mds.870100104</idno><idno type="ArticleID">MDS870100104</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cerebellar ataxia</term><term>Dihydroxyphenylalanine decarboxylase</term><term>Dominantly inherited olivopontocerebellar atrophy</term><term>Dopamine</term><term>Parkinson's disease</term><term>Tyrosine hydroxylase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We measured the levels of dopamine, tyrosine hydroxylase (TH) protein, and dihydroxyphenylalanine (DOPA) decarboxylase (DDC) protein in the striatum of 10 patients with idiopathic Parkinson's disease (PD) and 23 patients with dominantly inherited olivopontocerebellar atrophy (OPCA). The levels of dopamine were markedly reduced (2% of control) in the striatum of the patients with PD, whereas striatal dopamine in the patients with OPCA ranged from normal (<60% of control) to moderately reduced (20–60% of control) to severely depleted (<20% of control). Both TH and DDC protein levels were significantly lower than those of the controls in the striatum of all of the patients with PD and in the subgroup of patients with OPCA having severely depleted dopamine. In contradistinction, TH but not DDC protein levels were reduced in those patients with OPCA having moderately reduced dopamine levels. This suggests that in the early stage of nigrostriatal dopamine neurone degeneration, DDC levels may be less susceptible to neurodegenerative influences than is TH synthesis or, alternatively, DDC synthesis may be more aggressively upregulated. Unexpectedly, from the blot immunolabeling analysis an additional DDC‐immunoreactive band of slightly lower apparent molecular mass was detected in two of the patients with PD and in 12 of the patients with OPCA. This additional DDC band, which was not present in any of the control subjects, may reflect posttranslational modification(s) of DDC related to the neurodegenerative process.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Xiao‐Hui Zhong</name><affiliations><json:string>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>John W. Haycock</name><affiliations><json:string>Department of Biochemistry and Molecular Biology, Louisiana State University Medical Center, New Orleans, Louisiana, U.S.A.</json:string></affiliations></json:item><json:item><name>Kathleen Shannak</name><affiliations><json:string>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Yves Robitaille</name><affiliations><json:string>Department of Neuropathology, University of Montreal, Montreal, Quebec, Canada</json:string></affiliations></json:item><json:item><name>Jonathan Fratkin</name><affiliations><json:string>Department of Pathology (Neuropathology), University of Mississippi, Jackson, Mississippi, U.S.A.</json:string></affiliations></json:item><json:item><name>Arnuf H. Koeppen</name><affiliations><json:string>Veterans Administration Medical Center, Albany, New York, U.S.A.</json:string></affiliations></json:item><json:item><name>Oleh Hornykiewicz</name><affiliations><json:string>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</json:string><json:string>Institute of Biochemical Pharmacology, University of Vienna, Vienna, Austria</json:string></affiliations></json:item><json:item><name>Dr. Kish</name><affiliations><json:string>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Dominantly inherited olivopontocerebellar atrophy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cerebellar ataxia</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>Tyrosine hydroxylase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dihydroxyphenylalanine decarboxylase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We measured the levels of dopamine, tyrosine hydroxylase (TH) protein, and dihydroxyphenylalanine (DOPA) decarboxylase (DDC) protein in the striatum of 10 patients with idiopathic Parkinson's disease (PD) and 23 patients with dominantly inherited olivopontocerebellar atrophy (OPCA). The levels of dopamine were markedly reduced (2% of control) in the striatum of the patients with PD, whereas striatal dopamine in the patients with OPCA ranged from normal (>60% of control) to moderately reduced (20–60% of control) to severely depleted (>20% of control). Both TH and DDC protein levels were significantly lower than those of the controls in the striatum of all of the patients with PD and in the subgroup of patients with OPCA having severely depleted dopamine. In contradistinction, TH but not DDC protein levels were reduced in those patients with OPCA having moderately reduced dopamine levels. This suggests that in the early stage of nigrostriatal dopamine neurone degeneration, DDC levels may be less susceptible to neurodegenerative influences than is TH synthesis or, alternatively, DDC synthesis may be more aggressively upregulated. Unexpectedly, from the blot immunolabeling analysis an additional DDC‐immunoreactive band of slightly lower apparent molecular mass was detected in two of the patients with PD and in 12 of the patients with OPCA. 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The levels of dopamine were markedly reduced (2% of control) in the striatum of the patients with PD, whereas striatal dopamine in the patients with OPCA ranged from normal (<60% of control) to moderately reduced (20–60% of control) to severely depleted (<20% of control). Both TH and DDC protein levels were significantly lower than those of the controls in the striatum of all of the patients with PD and in the subgroup of patients with OPCA having severely depleted dopamine. In contradistinction, TH but not DDC protein levels were reduced in those patients with OPCA having moderately reduced dopamine levels. This suggests that in the early stage of nigrostriatal dopamine neurone degeneration, DDC levels may be less susceptible to neurodegenerative influences than is TH synthesis or, alternatively, DDC synthesis may be more aggressively upregulated. Unexpectedly, from the blot immunolabeling analysis an additional DDC‐immunoreactive band of slightly lower apparent molecular mass was detected in two of the patients with PD and in 12 of the patients with OPCA. This additional DDC band, which was not present in any of the control subjects, may reflect posttranslational modification(s) of DDC related to the neurodegenerative process.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Dominantly inherited olivopontocerebellar atrophy</term></item><item><term>Cerebellar ataxia</term></item><item><term>Dopamine</term></item><item><term>Tyrosine hydroxylase</term></item><item><term>Dihydroxyphenylalanine decarboxylase</term></item><item><term>Parkinson's disease</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1994-06-04">Registration</change><change when="1995-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/34AD1A9AA121CA42789265D7FF5002FA00623C49/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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affiliationRef="#af3"><personName><givenNames>Yves</givenNames><familyName>Robitaille</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Jonathan</givenNames><familyName>Fratkin</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Arnuf H.</givenNames><familyName>Koeppen</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1 #af6"><personName><givenNames>Oleh</givenNames><familyName>Hornykiewicz</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>Stephen J.</givenNames><familyName>Kish</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Biochemistry and Molecular Biology, Louisiana State University Medical Center, New Orleans, Louisiana, U.S.A.</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>Department of Neuropathology, University of Montreal, Montreal, Quebec, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Department of Pathology (Neuropathology), University of Mississippi, Jackson, Mississippi, U.S.A.</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Veterans Administration Medical Center, Albany, New York, U.S.A.</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="AT" type="organization"><unparsedAffiliation>Institute of Biochemical Pharmacology, University of Vienna, Vienna, Austria</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Dominantly inherited olivopontocerebellar atrophy</keyword><keyword xml:id="kwd2">Cerebellar ataxia</keyword><keyword xml:id="kwd3">Dopamine</keyword><keyword xml:id="kwd4">Tyrosine hydroxylase</keyword><keyword xml:id="kwd5">Dihydroxyphenylalanine decarboxylase</keyword><keyword xml:id="kwd6">Parkinson's disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We measured the levels of dopamine, tyrosine hydroxylase (TH) protein, and dihydroxyphenylalanine (DOPA) decarboxylase (DDC) protein in the striatum of 10 patients with idiopathic Parkinson's disease (PD) and 23 patients with dominantly inherited olivopontocerebellar atrophy (OPCA). The levels of dopamine were markedly reduced (2% of control) in the striatum of the patients with PD, whereas striatal dopamine in the patients with OPCA ranged from normal (<60% of control) to moderately reduced (20–60% of control) to severely depleted (<20% of control). Both TH and DDC protein levels were significantly lower than those of the controls in the striatum of all of the patients with PD and in the subgroup of patients with OPCA having severely depleted dopamine. In contradistinction, TH but not DDC protein levels were reduced in those patients with OPCA having moderately reduced dopamine levels. This suggests that in the early stage of nigrostriatal dopamine neurone degeneration, DDC levels may be less susceptible to neurodegenerative influences than is TH synthesis or, alternatively, DDC synthesis may be more aggressively upregulated. Unexpectedly, from the blot immunolabeling analysis an additional DDC‐immunoreactive band of slightly lower apparent molecular mass was detected in two of the patients with PD and in 12 of the patients with OPCA. This additional DDC band, which was not present in any of the control subjects, may reflect posttranslational modification(s) of DDC related to the neurodegenerative process.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Striatal dihydroxyphenylalanine decarboxylase and tyrosine hydroxylase protein in idiopathic Parkinson's disease and dominantly inherited olivopontocerebellar atrophy</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PARKINSON'S DISEASE AND OLIVOPONTOCEREBELLAR ATROPHY</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Striatal dihydroxyphenylalanine decarboxylase and tyrosine hydroxylase protein in idiopathic Parkinson's disease and dominantly inherited olivopontocerebellar atrophy</title></titleInfo><name type="personal"><namePart type="given">Xiao‐Hui</namePart><namePart type="family">Zhong</namePart><affiliation>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John W.</namePart><namePart type="family">Haycock</namePart><affiliation>Department of Biochemistry and Molecular Biology, Louisiana State University Medical Center, New Orleans, Louisiana, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kathleen</namePart><namePart type="family">Shannak</namePart><affiliation>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yves</namePart><namePart type="family">Robitaille</namePart><affiliation>Department of Neuropathology, University of Montreal, Montreal, Quebec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jonathan</namePart><namePart type="family">Fratkin</namePart><affiliation>Department of Pathology (Neuropathology), University of Mississippi, Jackson, Mississippi, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Arnuf H.</namePart><namePart type="family">Koeppen</namePart><affiliation>Veterans Administration Medical Center, Albany, New York, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Oleh</namePart><namePart type="family">Hornykiewicz</namePart><affiliation>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</affiliation><affiliation>Institute of Biochemical Pharmacology, University of Vienna, Vienna, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Kish</namePart><affiliation>Human Neurochemical Pathology laboratory, clarke Institute of Psychiatry, Toronto, Ontario, Canada</affiliation><description>Correspondence: Human Neurochemical Pathology Laboratory, Clarke Institute of Psychiatry, 250 College Street, Toronto, Ontario, Canada M5T 1R8</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1995-01</dateIssued><dateValid encoding="w3cdtf">1994-06-04</dateValid><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">1</extent><extent unit="references">26</extent></physicalDescription><abstract lang="en">We measured the levels of dopamine, tyrosine hydroxylase (TH) protein, and dihydroxyphenylalanine (DOPA) decarboxylase (DDC) protein in the striatum of 10 patients with idiopathic Parkinson's disease (PD) and 23 patients with dominantly inherited olivopontocerebellar atrophy (OPCA). The levels of dopamine were markedly reduced (2% of control) in the striatum of the patients with PD, whereas striatal dopamine in the patients with OPCA ranged from normal (<60% of control) to moderately reduced (20–60% of control) to severely depleted (<20% of control). Both TH and DDC protein levels were significantly lower than those of the controls in the striatum of all of the patients with PD and in the subgroup of patients with OPCA having severely depleted dopamine. In contradistinction, TH but not DDC protein levels were reduced in those patients with OPCA having moderately reduced dopamine levels. This suggests that in the early stage of nigrostriatal dopamine neurone degeneration, DDC levels may be less susceptible to neurodegenerative influences than is TH synthesis or, alternatively, DDC synthesis may be more aggressively upregulated. Unexpectedly, from the blot immunolabeling analysis an additional DDC‐immunoreactive band of slightly lower apparent molecular mass was detected in two of the patients with PD and in 12 of the patients with OPCA. This additional DDC band, which was not present in any of the control subjects, may reflect posttranslational modification(s) of DDC related to the neurodegenerative process.</abstract><subject lang="en"><genre>Keywords</genre><topic>Dominantly inherited olivopontocerebellar atrophy</topic><topic>Cerebellar ataxia</topic><topic>Dopamine</topic><topic>Tyrosine hydroxylase</topic><topic>Dihydroxyphenylalanine decarboxylase</topic><topic>Parkinson's disease</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>1995</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>10</start><end>17</end><total>8</total></extent></part></relatedItem><identifier type="istex">34AD1A9AA121CA42789265D7FF5002FA00623C49</identifier><identifier type="DOI">10.1002/mds.870100104</identifier><identifier type="ArticleID">MDS870100104</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1995 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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