Parkin immunoreactivity in the brain of human and non‐human primates: An immunohistochemical analysis in normal conditions and in Parkinsonian syndromes
Identifieur interne : 001045 ( Main/Corpus ); précédent : 001044; suivant : 001046Parkin immunoreactivity in the brain of human and non‐human primates: An immunohistochemical analysis in normal conditions and in Parkinsonian syndromes
Auteurs : Martin Zarate-Lagunes ; Wen-Jie Gu ; Véronique Blanchard ; Chantal Francois ; Marie-Paule Muriel ; Annick Mouatt-Prigent ; Bruno Bonici ; André Parent ; Andreas Hartmann ; Jérôme Yelnik ; Georg A. Boehme ; Laurent Pradier ; Saliha Moussaoui ; Baptiste Faucheux ; Rita Raisman-Vozari ; Yves Agid ; Alexis Brice ; Etienne C. HirschSource :
- Journal of Comparative Neurology [ 0021-9967 ] ; 2001-04-02.
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- KwdEn :
Abstract
The etiology of Parkinson's disease is unknown, but the gene involved in an autosomic recessive form of the disease with early onset has recently been identified. It codes for a protein with an unknown function called parkin. In the present study we produced a specific polyclonal antiserum against human parkin. Immunohistochemical analysis showed that parkin is expressed in neuronal perikarya and processes but also in glial and blood vessels in the primate brain (human and monkey). Electron microscopy indicated that parkin immunoreactivity is mostly located in large cytoplasmic vesicles and at the level of the endoplasmic reticulum. Parkin was expressed heterogeneously in various structures of the brain. It was detectable in the dopaminergic systems at the level of the perikarya in the mesencephalon but also in the striatum. However, parkin was also expressed by numerous nondopaminergic neurons. The staining intensity of parkin was particularly high in the hippocampal formation, the pallidal complex, the red nucleus, and the cerebellum. Comparison of control subjects with patients with Parkinson's disease and control animals with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐intoxicated animals revealed a loss of parkin‐immunoreactive neurons only in the substantia nigra pars compacta. Furthermore, the surviving dopaminergic neurons in the parkinsonian state continued to express parkin at a level similar to that observed in the control situation. These data indicate that parkin is a widely expressed protein. Thus, the degeneration of dopaminergic neurons in familial cases of Parkinson's disease with autosomal recessive transmission cannot be explained solely in terms of an alteration of this protein. J. Comp. Neurol. 432:184–196, 2001. © 2001 Wiley‐Liss, Inc.
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DOI: 10.1002/cne.1096
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Hirsch</name><affiliation><mods:affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Comparative Neurology</title><title level="j" type="abbrev">J. Comp. Neurol.</title><idno type="ISSN">0021-9967</idno><idno type="eISSN">1096-9861</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-04-02">2001-04-02</date><biblScope unit="volume">432</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="184">184</biblScope><biblScope unit="page" to="196">196</biblScope></imprint><idno type="ISSN">0021-9967</idno></series><idno type="istex">25FAC305157A4B16A81C30141173AE2F51B97ADD</idno><idno type="DOI">10.1002/cne.1096</idno><idno type="ArticleID">CNE1096</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0021-9967</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinsonism</term><term>antibody</term><term>cell death</term><term>genetic</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The etiology of Parkinson's disease is unknown, but the gene involved in an autosomic recessive form of the disease with early onset has recently been identified. It codes for a protein with an unknown function called parkin. In the present study we produced a specific polyclonal antiserum against human parkin. Immunohistochemical analysis showed that parkin is expressed in neuronal perikarya and processes but also in glial and blood vessels in the primate brain (human and monkey). Electron microscopy indicated that parkin immunoreactivity is mostly located in large cytoplasmic vesicles and at the level of the endoplasmic reticulum. Parkin was expressed heterogeneously in various structures of the brain. It was detectable in the dopaminergic systems at the level of the perikarya in the mesencephalon but also in the striatum. However, parkin was also expressed by numerous nondopaminergic neurons. The staining intensity of parkin was particularly high in the hippocampal formation, the pallidal complex, the red nucleus, and the cerebellum. Comparison of control subjects with patients with Parkinson's disease and control animals with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐intoxicated animals revealed a loss of parkin‐immunoreactive neurons only in the substantia nigra pars compacta. Furthermore, the surviving dopaminergic neurons in the parkinsonian state continued to express parkin at a level similar to that observed in the control situation. These data indicate that parkin is a widely expressed protein. Thus, the degeneration of dopaminergic neurons in familial cases of Parkinson's disease with autosomal recessive transmission cannot be explained solely in terms of an alteration of this protein. J. Comp. Neurol. 432:184–196, 2001. © 2001 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Martin Zarate‐Lagunes</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Wen‐Jie Gu</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Véronique Blanchard</name><affiliations><json:string>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</json:string></affiliations></json:item><json:item><name>Chantal Francois</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Marie‐Paule Muriel</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Annick Mouatt‐Prigent</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Bruno Bonici</name><affiliations><json:string>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</json:string></affiliations></json:item><json:item><name>André Parent</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Andreas Hartmann</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Jérôme Yelnik</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Georg A. Boehme</name><affiliations><json:string>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</json:string></affiliations></json:item><json:item><name>Laurent Pradier</name><affiliations><json:string>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</json:string></affiliations></json:item><json:item><name>Saliha Moussaoui</name><affiliations><json:string>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</json:string></affiliations></json:item><json:item><name>Baptiste Faucheux</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Rita Raisman‐Vozari</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Yves Agid</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Alexis Brice</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Etienne C. Hirsch</name><affiliations><json:string>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>antibody</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinsonism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cell death</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>genetic</value></json:item></subject><articleId><json:string>CNE1096</json:string></articleId><language><json:string>eng</json:string></language><abstract>The etiology of Parkinson's disease is unknown, but the gene involved in an autosomic recessive form of the disease with early onset has recently been identified. It codes for a protein with an unknown function called parkin. In the present study we produced a specific polyclonal antiserum against human parkin. Immunohistochemical analysis showed that parkin is expressed in neuronal perikarya and processes but also in glial and blood vessels in the primate brain (human and monkey). Electron microscopy indicated that parkin immunoreactivity is mostly located in large cytoplasmic vesicles and at the level of the endoplasmic reticulum. Parkin was expressed heterogeneously in various structures of the brain. It was detectable in the dopaminergic systems at the level of the perikarya in the mesencephalon but also in the striatum. However, parkin was also expressed by numerous nondopaminergic neurons. The staining intensity of parkin was particularly high in the hippocampal formation, the pallidal complex, the red nucleus, and the cerebellum. Comparison of control subjects with patients with Parkinson's disease and control animals with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐intoxicated animals revealed a loss of parkin‐immunoreactive neurons only in the substantia nigra pars compacta. Furthermore, the surviving dopaminergic neurons in the parkinsonian state continued to express parkin at a level similar to that observed in the control situation. These data indicate that parkin is a widely expressed protein. Thus, the degeneration of dopaminergic neurons in familial cases of Parkinson's disease with autosomal recessive transmission cannot be explained solely in terms of an alteration of this protein. J. Comp. Neurol. 432:184–196, 2001. © 2001 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>8</score><pdfVersion>1.2</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1795</abstractCharCount><pdfWordCount>7576</pdfWordCount><pdfCharCount>47394</pdfCharCount><pdfPageCount>13</pdfPageCount><abstractWordCount>258</abstractWordCount></qualityIndicators><title>Parkin immunoreactivity in the brain of human and non‐human primates: An immunohistochemical analysis in normal conditions and in Parkinsonian 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Parkinsonian syndromes</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><availability><p>WILEY</p></availability><date>2001</date></publicationStmt><notesStmt><note>INSERM (Institut National de la Santé et de la Recherche Médicale, Paris, France)</note><note>The French Parkinson Association (Paris, France)</note><note>Avantis Pharma (Vitry‐sur‐Seine, France)</note><note>National Parkinson Disease Foundation (Miami, FL)</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Parkin immunoreactivity in the brain of human and non‐human primates: An immunohistochemical analysis in normal conditions and in Parkinsonian syndromes</title><author><persName><forename type="first">Martin</forename><surname>Zarate‐Lagunes</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Wen‐Jie</forename><surname>Gu</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Véronique</forename><surname>Blanchard</surname></persName><affiliation>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</affiliation></author><author><persName><forename type="first">Chantal</forename><surname>Francois</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Marie‐Paule</forename><surname>Muriel</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Annick</forename><surname>Mouatt‐Prigent</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Bruno</forename><surname>Bonici</surname></persName><affiliation>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</affiliation></author><author><persName><forename type="first">André</forename><surname>Parent</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Andreas</forename><surname>Hartmann</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Jérôme</forename><surname>Yelnik</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Georg A.</forename><surname>Boehme</surname></persName><affiliation>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</affiliation></author><author><persName><forename type="first">Laurent</forename><surname>Pradier</surname></persName><affiliation>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</affiliation></author><author><persName><forename type="first">Saliha</forename><surname>Moussaoui</surname></persName><affiliation>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</affiliation></author><author><persName><forename type="first">Baptiste</forename><surname>Faucheux</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Rita</forename><surname>Raisman‐Vozari</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Yves</forename><surname>Agid</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Alexis</forename><surname>Brice</surname></persName><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author><author><persName><forename type="first">Etienne C.</forename><surname>Hirsch</surname></persName><note type="correspondence"><p>Correspondence: INSERM U289, Hôpital de la Salpêtrière, 47 Bd. de l'Hôpital, 75013 Paris, France</p></note><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation></author></analytic><monogr><title level="j">Journal of Comparative Neurology</title><title level="j" type="abbrev">J. Comp. Neurol.</title><idno type="pISSN">0021-9967</idno><idno type="eISSN">1096-9861</idno><idno type="DOI">10.1002/(ISSN)1096-9861</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-04-02"></date><biblScope unit="volume">432</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="184">184</biblScope><biblScope unit="page" to="196">196</biblScope></imprint></monogr><idno type="istex">25FAC305157A4B16A81C30141173AE2F51B97ADD</idno><idno type="DOI">10.1002/cne.1096</idno><idno type="ArticleID">CNE1096</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2001</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The etiology of Parkinson's disease is unknown, but the gene involved in an autosomic recessive form of the disease with early onset has recently been identified. It codes for a protein with an unknown function called parkin. In the present study we produced a specific polyclonal antiserum against human parkin. Immunohistochemical analysis showed that parkin is expressed in neuronal perikarya and processes but also in glial and blood vessels in the primate brain (human and monkey). Electron microscopy indicated that parkin immunoreactivity is mostly located in large cytoplasmic vesicles and at the level of the endoplasmic reticulum. Parkin was expressed heterogeneously in various structures of the brain. It was detectable in the dopaminergic systems at the level of the perikarya in the mesencephalon but also in the striatum. However, parkin was also expressed by numerous nondopaminergic neurons. The staining intensity of parkin was particularly high in the hippocampal formation, the pallidal complex, the red nucleus, and the cerebellum. Comparison of control subjects with patients with Parkinson's disease and control animals with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐intoxicated animals revealed a loss of parkin‐immunoreactive neurons only in the substantia nigra pars compacta. Furthermore, the surviving dopaminergic neurons in the parkinsonian state continued to express parkin at a level similar to that observed in the control situation. These data indicate that parkin is a widely expressed protein. Thus, the degeneration of dopaminergic neurons in familial cases of Parkinson's disease with autosomal recessive transmission cannot be explained solely in terms of an alteration of this protein. J. Comp. Neurol. 432:184–196, 2001. © 2001 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>antibody</term></item><item><term>Parkinsonism</term></item><item><term>cell death</term></item><item><term>genetic</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="2000-02-29">Received</change><change when="2000-12-21">Registration</change><change when="2001-04-02">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/25FAC305157A4B16A81C30141173AE2F51B97ADD/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>John Wiley & Sons, Inc.</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1096-9861</doi><issn type="print">0021-9967</issn><issn type="electronic">1096-9861</issn><idGroup><id type="product" value="CNE"></id></idGroup><titleGroup><title type="main" xml:lang="en">Journal of Comparative Neurology</title><title type="short">J. 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number="2"></count><count type="referenceTotal" number="27"></count><count type="wordTotal" number="8736"></count></countGroup><titleGroup><title type="main" xml:lang="en">Parkin immunoreactivity in the brain of human and non‐human primates: An immunohistochemical analysis in normal conditions and in Parkinsonian syndromes</title><title type="short" xml:lang="en">Parkin in Primate Brain</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Martin</givenNames><familyName>Zarate‐Lagunes</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Wen‐Jie</givenNames><familyName>Gu</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Véronique</givenNames><familyName>Blanchard</familyName></personName></creator><creator xml:id="au4" creatorRole="author" 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type="author"><keyword xml:id="kwd1">antibody</keyword><keyword xml:id="kwd2">Parkinsonism</keyword><keyword xml:id="kwd3">cell death</keyword><keyword xml:id="kwd4">genetic</keyword></keywordGroup><fundingInfo><fundingAgency>INSERM (Institut National de la Santé et de la Recherche Médicale, Paris, France)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>The French Parkinson Association (Paris, France)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Avantis Pharma (Vitry‐sur‐Seine, France)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>National Parkinson Disease Foundation (Miami, FL)</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The etiology of Parkinson's disease is unknown, but the gene involved in an autosomic recessive form of the disease with early onset has recently been identified. It codes for a protein with an unknown function called parkin. In the present study we produced a specific polyclonal antiserum against human parkin. Immunohistochemical analysis showed that parkin is expressed in neuronal perikarya and processes but also in glial and blood vessels in the primate brain (human and monkey). Electron microscopy indicated that parkin immunoreactivity is mostly located in large cytoplasmic vesicles and at the level of the endoplasmic reticulum. Parkin was expressed heterogeneously in various structures of the brain. It was detectable in the dopaminergic systems at the level of the perikarya in the mesencephalon but also in the striatum. However, parkin was also expressed by numerous nondopaminergic neurons. The staining intensity of parkin was particularly high in the hippocampal formation, the pallidal complex, the red nucleus, and the cerebellum. Comparison of control subjects with patients with Parkinson's disease and control animals with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐intoxicated animals revealed a loss of parkin‐immunoreactive neurons only in the substantia nigra pars compacta. Furthermore, the surviving dopaminergic neurons in the parkinsonian state continued to express parkin at a level similar to that observed in the control situation. These data indicate that parkin is a widely expressed protein. Thus, the degeneration of dopaminergic neurons in familial cases of Parkinson's disease with autosomal recessive transmission cannot be explained solely in terms of an alteration of this protein. J. Comp. Neurol. 432:184–196, 2001. © 2001 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Parkin immunoreactivity in the brain of human and non‐human primates: An immunohistochemical analysis in normal conditions and in Parkinsonian syndromes</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Parkin in Primate Brain</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Parkin immunoreactivity in the brain of human and non‐human primates: An immunohistochemical analysis in normal conditions and in Parkinsonian syndromes</title></titleInfo><name type="personal"><namePart type="given">Martin</namePart><namePart type="family">Zarate‐Lagunes</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wen‐Jie</namePart><namePart type="family">Gu</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Véronique</namePart><namePart type="family">Blanchard</namePart><affiliation>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chantal</namePart><namePart type="family">Francois</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marie‐Paule</namePart><namePart type="family">Muriel</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Annick</namePart><namePart type="family">Mouatt‐Prigent</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bruno</namePart><namePart type="family">Bonici</namePart><affiliation>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">André</namePart><namePart type="family">Parent</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andreas</namePart><namePart type="family">Hartmann</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jérôme</namePart><namePart type="family">Yelnik</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Georg A.</namePart><namePart type="family">Boehme</namePart><affiliation>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Laurent</namePart><namePart type="family">Pradier</namePart><affiliation>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Saliha</namePart><namePart type="family">Moussaoui</namePart><affiliation>Neurodegenerative Diseases, Avantis Pharma, 94403 Vitry‐Sur‐Seine, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Baptiste</namePart><namePart type="family">Faucheux</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rita</namePart><namePart type="family">Raisman‐Vozari</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yves</namePart><namePart type="family">Agid</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alexis</namePart><namePart type="family">Brice</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Etienne C.</namePart><namePart type="family">Hirsch</namePart><affiliation>INSERM U 289, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><description>Correspondence: INSERM U289, Hôpital de la Salpêtrière, 47 Bd. de l'Hôpital, 75013 Paris, France</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2001-04-02</dateIssued><dateCaptured encoding="w3cdtf">2000-02-29</dateCaptured><dateValid encoding="w3cdtf">2000-12-21</dateValid><copyrightDate encoding="w3cdtf">2001</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">10</extent><extent unit="tables">2</extent><extent unit="references">27</extent><extent unit="words">8736</extent></physicalDescription><abstract lang="en">The etiology of Parkinson's disease is unknown, but the gene involved in an autosomic recessive form of the disease with early onset has recently been identified. It codes for a protein with an unknown function called parkin. In the present study we produced a specific polyclonal antiserum against human parkin. Immunohistochemical analysis showed that parkin is expressed in neuronal perikarya and processes but also in glial and blood vessels in the primate brain (human and monkey). Electron microscopy indicated that parkin immunoreactivity is mostly located in large cytoplasmic vesicles and at the level of the endoplasmic reticulum. Parkin was expressed heterogeneously in various structures of the brain. It was detectable in the dopaminergic systems at the level of the perikarya in the mesencephalon but also in the striatum. However, parkin was also expressed by numerous nondopaminergic neurons. The staining intensity of parkin was particularly high in the hippocampal formation, the pallidal complex, the red nucleus, and the cerebellum. Comparison of control subjects with patients with Parkinson's disease and control animals with 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐intoxicated animals revealed a loss of parkin‐immunoreactive neurons only in the substantia nigra pars compacta. Furthermore, the surviving dopaminergic neurons in the parkinsonian state continued to express parkin at a level similar to that observed in the control situation. These data indicate that parkin is a widely expressed protein. Thus, the degeneration of dopaminergic neurons in familial cases of Parkinson's disease with autosomal recessive transmission cannot be explained solely in terms of an alteration of this protein. J. Comp. Neurol. 432:184–196, 2001. © 2001 Wiley‐Liss, Inc.</abstract><note type="funding">INSERM (Institut National de la Santé et de la Recherche Médicale, Paris, France)</note><note type="funding">The French Parkinson Association (Paris, France)</note><note type="funding">Avantis Pharma (Vitry‐sur‐Seine, France)</note><note type="funding">National Parkinson Disease Foundation (Miami, FL)</note><subject lang="en"><genre>Keywords</genre><topic>antibody</topic><topic>Parkinsonism</topic><topic>cell death</topic><topic>genetic</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Comparative Neurology</title></titleInfo><titleInfo type="abbreviated"><title>J. Comp. 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