Cellular Expression of α7 Nicotinic Acetylcholine Receptor Protein in the Temporal Cortex in Alzheimer's and Parkinson's Disease— A Stereological Approach
Identifieur interne : 002C54 ( Main/Corpus ); précédent : 002C53; suivant : 002C55Cellular Expression of α7 Nicotinic Acetylcholine Receptor Protein in the Temporal Cortex in Alzheimer's and Parkinson's Disease— A Stereological Approach
Auteurs : Carolin Banerjee ; Jens R. Nyengaard ; Andrea Wevers ; Rob A. I. De Vos ; Ernst N. H. Jansen Steur ; Jon Lindstrom ; Kirsten Pilz ; Sonja Nowacki ; Wilhelm Bloch ; Hannsjörg SchröderSource :
- Neurobiology of Disease [ 0969-9961 ] ; 2000.
Abstract
Cognitive deficits in Alzheimer's and Parkinson's disease are closely related to disturbed cholinergic transmission. The decrease of nicotinic acetylcholine receptor protein has been assessed by Western blotting and immunohistochemistry. Stereology, however, has not been used to assess numbers of receptor-expressing human cerebrocortical neurons. Our approach applies a combination of α7 subunit-immunohistochemistry with a stereological technique using defined stretches of pial surface as reference standard. The number of α7 subunit protein-expressing neurons in the Alzheimer temporal cortices amounted to approximately half of that of controls while numbers in Parkinson patients lay in between. No differences in the total number of neurons were seen. These results corroborate nonstereological studies on Alzheimer cortices and for the first time show a similar decrease in receptor expression in Parkinson's disease. They provide evidence that not only Alzheimer dementia but also cognitive deficits in Parkinson's disease may be related to decreased nicotinic receptor expression.
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DOI: 10.1006/nbdi.2000.0317
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Germany</mods:affiliation></affiliation></author><author><name sortKey="Nowacki, Sonja" sort="Nowacki, Sonja" uniqKey="Nowacki S" first="Sonja" last="Nowacki">Sonja Nowacki</name><affiliation><mods:affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</mods:affiliation></affiliation></author><author><name sortKey="Bloch, Wilhelm" sort="Bloch, Wilhelm" uniqKey="Bloch W" first="Wilhelm" last="Bloch">Wilhelm Bloch</name><affiliation><mods:affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</mods:affiliation></affiliation></author><author><name sortKey="Schroder, Hannsjorg" sort="Schroder, Hannsjorg" uniqKey="Schroder H" first="Hannsjörg" last="Schröder">Hannsjörg Schröder</name><affiliation><mods:affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. 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Germany</mods:affiliation></affiliation></author><author><name sortKey="Nyengaard, Jens R" sort="Nyengaard, Jens R" uniqKey="Nyengaard J" first="Jens R." last="Nyengaard">Jens R. Nyengaard</name><affiliation><mods:affiliation>Stereological Research Laboratory, University of Aarhus, DK-8000, Aarhus C, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Wevers, Andrea" sort="Wevers, Andrea" uniqKey="Wevers A" first="Andrea" last="Wevers">Andrea Wevers</name><affiliation><mods:affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</mods:affiliation></affiliation></author><author><name sortKey="De Vos, Rob A I" sort="De Vos, Rob A I" uniqKey="De Vos R" first="Rob A. I." last="De Vos">Rob A. I. De Vos</name><affiliation><mods:affiliation>Laboratorium Pathologie Oost Nederland, Enschede, NL-7512 AD, Enschede, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Jansen Steur, Ernst N H" sort="Jansen Steur, Ernst N H" uniqKey="Jansen Steur E" first="Ernst N. H." last="Jansen Steur">Ernst N. H. Jansen Steur</name><affiliation><mods:affiliation>Department of Neurology, Medisch Spectrum Twente, NL-7500 KA, Enschede, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Lindstrom, Jon" sort="Lindstrom, Jon" uniqKey="Lindstrom J" first="Jon" last="Lindstrom">Jon Lindstrom</name><affiliation><mods:affiliation>University of Pennsylvania School of Medicine, Department of Neuroscience, 215 Stemmler Hall, Philadelphia, Pennsylvania, 19104-6074</mods:affiliation></affiliation></author><author><name sortKey="Pilz, Kirsten" sort="Pilz, Kirsten" uniqKey="Pilz K" first="Kirsten" last="Pilz">Kirsten Pilz</name><affiliation><mods:affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</mods:affiliation></affiliation></author><author><name sortKey="Nowacki, Sonja" sort="Nowacki, Sonja" uniqKey="Nowacki S" first="Sonja" last="Nowacki">Sonja Nowacki</name><affiliation><mods:affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</mods:affiliation></affiliation></author><author><name sortKey="Bloch, Wilhelm" sort="Bloch, Wilhelm" uniqKey="Bloch W" first="Wilhelm" last="Bloch">Wilhelm Bloch</name><affiliation><mods:affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</mods:affiliation></affiliation></author><author><name sortKey="Schroder, Hannsjorg" sort="Schroder, Hannsjorg" uniqKey="Schroder H" first="Hannsjörg" last="Schröder">Hannsjörg Schröder</name><affiliation><mods:affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Neurobiology of Disease</title><title level="j" type="abbrev">YNBDI</title><idno type="ISSN">0969-9961</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">7</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="666">666</biblScope><biblScope unit="page" to="672">672</biblScope></imprint><idno type="ISSN">0969-9961</idno></series><idno type="istex">33754962D7A2449E6AE2C606E739A08D49AE5BEF</idno><idno type="DOI">10.1006/nbdi.2000.0317</idno><idno type="PII">S0969-9961(00)90317-6</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0969-9961</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cognitive deficits in Alzheimer's and Parkinson's disease are closely related to disturbed cholinergic transmission. The decrease of nicotinic acetylcholine receptor protein has been assessed by Western blotting and immunohistochemistry. Stereology, however, has not been used to assess numbers of receptor-expressing human cerebrocortical neurons. Our approach applies a combination of α7 subunit-immunohistochemistry with a stereological technique using defined stretches of pial surface as reference standard. The number of α7 subunit protein-expressing neurons in the Alzheimer temporal cortices amounted to approximately half of that of controls while numbers in Parkinson patients lay in between. No differences in the total number of neurons were seen. These results corroborate nonstereological studies on Alzheimer cortices and for the first time show a similar decrease in receptor expression in Parkinson's disease. They provide evidence that not only Alzheimer dementia but also cognitive deficits in Parkinson's disease may be related to decreased nicotinic receptor expression.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Carolin Banerjee</name><affiliations><json:string>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</json:string></affiliations></json:item><json:item><name>Jens R. Nyengaard</name><affiliations><json:string>Stereological Research Laboratory, University of Aarhus, DK-8000, Aarhus C, Denmark</json:string></affiliations></json:item><json:item><name>Andrea Wevers</name><affiliations><json:string>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</json:string></affiliations></json:item><json:item><name>Rob A.I. de Vos</name><affiliations><json:string>Laboratorium Pathologie Oost Nederland, Enschede, NL-7512 AD, Enschede, The Netherlands</json:string></affiliations></json:item><json:item><name>Ernst N.H. Jansen Steur</name><affiliations><json:string>Department of Neurology, Medisch Spectrum Twente, NL-7500 KA, Enschede, The Netherlands</json:string></affiliations></json:item><json:item><name>Jon Lindstrom</name><affiliations><json:string>University of Pennsylvania School of Medicine, Department of Neuroscience, 215 Stemmler Hall, Philadelphia, Pennsylvania, 19104-6074</json:string></affiliations></json:item><json:item><name>Kirsten Pilz</name><affiliations><json:string>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</json:string></affiliations></json:item><json:item><name>Sonja Nowacki</name><affiliations><json:string>Department of Anatomy, University of Köln, D-50924, Köln, F. R. 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The number of α7 subunit protein-expressing neurons in the Alzheimer temporal cortices amounted to approximately half of that of controls while numbers in Parkinson patients lay in between. No differences in the total number of neurons were seen. These results corroborate nonstereological studies on Alzheimer cortices and for the first time show a similar decrease in receptor expression in Parkinson's disease. 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R. Germany</affiliation></author><author><persName><forename type="first">Jens R.</forename><surname>Nyengaard</surname></persName><affiliation>Stereological Research Laboratory, University of Aarhus, DK-8000, Aarhus C, Denmark</affiliation></author><author><persName><forename type="first">Andrea</forename><surname>Wevers</surname></persName><affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. 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Germany</affiliation></author></analytic><monogr><title level="j">Neurobiology of Disease</title><title level="j" type="abbrev">YNBDI</title><idno type="pISSN">0969-9961</idno><idno type="PII">S0969-9961(00)X0011-3</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000"></date><biblScope unit="volume">7</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="666">666</biblScope><biblScope unit="page" to="672">672</biblScope></imprint></monogr><idno type="istex">33754962D7A2449E6AE2C606E739A08D49AE5BEF</idno><idno type="DOI">10.1006/nbdi.2000.0317</idno><idno type="PII">S0969-9961(00)90317-6</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2000</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Cognitive deficits in Alzheimer's and Parkinson's disease are closely related to disturbed cholinergic transmission. The decrease of nicotinic acetylcholine receptor protein has been assessed by Western blotting and immunohistochemistry. Stereology, however, has not been used to assess numbers of receptor-expressing human cerebrocortical neurons. Our approach applies a combination of α7 subunit-immunohistochemistry with a stereological technique using defined stretches of pial surface as reference standard. The number of α7 subunit protein-expressing neurons in the Alzheimer temporal cortices amounted to approximately half of that of controls while numbers in Parkinson patients lay in between. No differences in the total number of neurons were seen. These results corroborate nonstereological studies on Alzheimer cortices and for the first time show a similar decrease in receptor expression in Parkinson's disease. They provide evidence that not only Alzheimer dementia but also cognitive deficits in Parkinson's disease may be related to decreased nicotinic receptor expression.</p></abstract></profileDesc><revisionDesc><change when="2000-06-19">Registration</change><change when="2000-06-15">Modified</change><change when="2000">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/33754962D7A2449E6AE2C606E739A08D49AE5BEF/fulltext/txt</uri></json:item></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" xml:lang="en"><item-info><jid>YNBDI</jid><aid>90317</aid><ce:pii>S0969-9961(00)90317-6</ce:pii><ce:doi>10.1006/nbdi.2000.0317</ce:doi><ce:copyright type="full-transfer" year="2000">Academic Press</ce:copyright></item-info><head><ce:dochead><ce:textfn>Regular Article</ce:textfn></ce:dochead><ce:title>Cellular Expression of α7 Nicotinic Acetylcholine Receptor Protein in the Temporal Cortex in Alzheimer's and Parkinson's Disease— A Stereological Approach</ce:title><ce:author-group><ce:author><ce:given-name>Carolin</ce:given-name><ce:surname>Banerjee</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Jens R.</ce:given-name><ce:surname>Nyengaard</ce:surname><ce:cross-ref refid="A2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Andrea</ce:given-name><ce:surname>Wevers</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Rob A.I.</ce:given-name><ce:surname>de Vos</ce:surname><ce:cross-ref refid="A3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Ernst N.H.</ce:given-name><ce:surname>Jansen Steur</ce:surname><ce:cross-ref refid="A4"><ce:sup>d</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Jon</ce:given-name><ce:surname>Lindstrom</ce:surname><ce:cross-ref refid="A5"><ce:sup>e</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Kirsten</ce:given-name><ce:surname>Pilz</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Sonja</ce:given-name><ce:surname>Nowacki</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Wilhelm</ce:given-name><ce:surname>Bloch</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Hannsjörg</ce:given-name><ce:surname>Schröder</ce:surname><ce:cross-ref refid="A1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="A1"><ce:label>a</ce:label><ce:textfn>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</ce:textfn></ce:affiliation><ce:affiliation id="A2"><ce:label>b</ce:label><ce:textfn>Stereological Research Laboratory, University of Aarhus, DK-8000, Aarhus C, Denmark</ce:textfn></ce:affiliation><ce:affiliation id="A3"><ce:label>c</ce:label><ce:textfn>Laboratorium Pathologie Oost Nederland, Enschede, NL-7512 AD, Enschede, The Netherlands</ce:textfn></ce:affiliation><ce:affiliation id="A4"><ce:label>d</ce:label><ce:textfn>Department of Neurology, Medisch Spectrum Twente, NL-7500 KA, Enschede, The Netherlands</ce:textfn></ce:affiliation><ce:affiliation id="A5"><ce:label>e</ce:label><ce:textfn>University of Pennsylvania School of Medicine, Department of Neuroscience, 215 Stemmler Hall, Philadelphia, Pennsylvania, 19104-6074</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="5" month="4" year="2000"></ce:date-received><ce:date-revised day="15" month="6" year="2000"></ce:date-revised><ce:date-accepted day="19" month="6" year="2000"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Cognitive deficits in Alzheimer's and Parkinson's disease are closely related to disturbed cholinergic transmission. The decrease of nicotinic acetylcholine receptor protein has been assessed by Western blotting and immunohistochemistry. Stereology, however, has not been used to assess numbers of receptor-expressing human cerebrocortical neurons. Our approach applies a combination of α7 subunit-immunohistochemistry with a stereological technique using defined stretches of pial surface as reference standard. The number of α7 subunit protein-expressing neurons in the Alzheimer temporal cortices amounted to approximately half of that of controls while numbers in Parkinson patients lay in between. No differences in the total number of neurons were seen. These results corroborate nonstereological studies on Alzheimer cortices and for the first time show a similar decrease in receptor expression in Parkinson's disease. They provide evidence that not only Alzheimer dementia but also cognitive deficits in Parkinson's disease may be related to decreased nicotinic receptor expression.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Cellular Expression of α7 Nicotinic Acetylcholine Receptor Protein in the Temporal Cortex in Alzheimer's and Parkinson's Disease— A Stereological Approach</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Cellular Expression of α7 Nicotinic Acetylcholine Receptor Protein in the Temporal Cortex in Alzheimer's and Parkinson's Disease— A Stereological Approach</title></titleInfo><name type="personal"><namePart type="given">Carolin</namePart><namePart type="family">Banerjee</namePart><affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jens R.</namePart><namePart type="family">Nyengaard</namePart><affiliation>Stereological Research Laboratory, University of Aarhus, DK-8000, Aarhus C, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrea</namePart><namePart type="family">Wevers</namePart><affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rob A.I.</namePart><namePart type="family">de Vos</namePart><affiliation>Laboratorium Pathologie Oost Nederland, Enschede, NL-7512 AD, Enschede, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ernst N.H.</namePart><namePart type="family">Jansen Steur</namePart><affiliation>Department of Neurology, Medisch Spectrum Twente, NL-7500 KA, Enschede, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jon</namePart><namePart type="family">Lindstrom</namePart><affiliation>University of Pennsylvania School of Medicine, Department of Neuroscience, 215 Stemmler Hall, Philadelphia, Pennsylvania, 19104-6074</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kirsten</namePart><namePart type="family">Pilz</namePart><affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sonja</namePart><namePart type="family">Nowacki</namePart><affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Wilhelm</namePart><namePart type="family">Bloch</namePart><affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hannsjörg</namePart><namePart type="family">Schröder</namePart><affiliation>Department of Anatomy, University of Köln, D-50924, Köln, F. R. Germany</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">2000</dateIssued><dateValid encoding="w3cdtf">2000-06-19</dateValid><dateModified encoding="w3cdtf">2000-06-15</dateModified><copyrightDate encoding="w3cdtf">2000</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">Cognitive deficits in Alzheimer's and Parkinson's disease are closely related to disturbed cholinergic transmission. The decrease of nicotinic acetylcholine receptor protein has been assessed by Western blotting and immunohistochemistry. Stereology, however, has not been used to assess numbers of receptor-expressing human cerebrocortical neurons. Our approach applies a combination of α7 subunit-immunohistochemistry with a stereological technique using defined stretches of pial surface as reference standard. The number of α7 subunit protein-expressing neurons in the Alzheimer temporal cortices amounted to approximately half of that of controls while numbers in Parkinson patients lay in between. No differences in the total number of neurons were seen. These results corroborate nonstereological studies on Alzheimer cortices and for the first time show a similar decrease in receptor expression in Parkinson's disease. They provide evidence that not only Alzheimer dementia but also cognitive deficits in Parkinson's disease may be related to decreased nicotinic receptor expression.</abstract><note type="content">Section title: Regular Article</note><relatedItem type="host"><titleInfo><title>Neurobiology of Disease</title></titleInfo><titleInfo type="abbreviated"><title>YNBDI</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">200012</dateIssued></originInfo><identifier type="ISSN">0969-9961</identifier><identifier type="PII">S0969-9961(00)X0011-3</identifier><part><date>200012</date><detail type="volume"><number>7</number><caption>vol.</caption></detail><detail type="issue"><number>6</number><caption>no.</caption></detail><extent unit="issue pages"><start>561</start><end>699</end></extent><extent unit="pages"><start>666</start><end>672</end></extent></part></relatedItem><identifier type="istex">33754962D7A2449E6AE2C606E739A08D49AE5BEF</identifier><identifier type="DOI">10.1006/nbdi.2000.0317</identifier><identifier type="PII">S0969-9961(00)90317-6</identifier><accessCondition type="use and reproduction" contentType="">© 2000Academic Press</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Academic Press, ©2000</recordOrigin></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/33754962D7A2449E6AE2C606E739A08D49AE5BEF/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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