Can Alzheimer's type pathology influence the clinical phenotype of Parkinson's disease?
Identifieur interne : 000708 ( Main/Corpus ); précédent : 000707; suivant : 000709Can Alzheimer's type pathology influence the clinical phenotype of Parkinson's disease?
Auteurs : S. Papapetropoulos ; A. Lieberman ; J. Gonzalez ; D. C. MashSource :
- Acta Neurologica Scandinavica [ 0001-6314 ] ; 2005-06.
English descriptors
Abstract
Objectives – Patients with clinical and pathological diagnosis of Parkinson's disease (PD) may, at death, also be found to have the pathological changes of Alzheimer's disease (AD). With this study we aim to determine the influence of AD pathology on the clinical phenotype of PD. Methods – We studied 64 patients who donated their brains to the University of Miami Brain Endowment BankTM and fulfilled the clinical and pathological criteria for PD. For the evaluation of AD pathology we used the CERAD criteria. Dementia was diagnosed, in life, also using standard criteria. Case histories were abstracted and reviewed by one investigator (SP) who then made comparisons between patients. Results – Patients with AD pathology (PD–AD) were older both at the time of diagnosis and death. The presence of AD pathology did not seem to influence disease duration in our cohort of PD patients. As expected there was a clear relation between AD pathology and dementia but not all PD–AD patients were demented. Psychosis and depression were also found to be more prevalent in the PD–AD patients. In the comparison between demented and non‐demented PD–AD patients dementia was more likely to appear in patients with PD and definite criteria for AD. Conclusion – Apart from dementia AD pathology seems to be associated with a number of other clinical characteristics of PD.
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DOI: 10.1111/j.1600-0404.2005.00411.x
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Lieberman</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>National Parkinson Foundation (NPF), Miami, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Gonzalez, J" sort="Gonzalez, J" uniqKey="Gonzalez J" first="J." last="Gonzalez">J. Gonzalez</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Mash, D C" sort="Mash, D C" uniqKey="Mash D" first="D. C." last="Mash">D. C. 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Papapetropoulos</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Lieberman, A" sort="Lieberman, A" uniqKey="Lieberman A" first="A." last="Lieberman">A. Lieberman</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>National Parkinson Foundation (NPF), Miami, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Gonzalez, J" sort="Gonzalez, J" uniqKey="Gonzalez J" first="J." last="Gonzalez">J. Gonzalez</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Mash, D C" sort="Mash, D C" uniqKey="Mash D" first="D. C." last="Mash">D. C. Mash</name><affiliation><mods:affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Acta Neurologica Scandinavica</title><idno type="ISSN">0001-6314</idno><idno type="eISSN">1600-0404</idno><imprint><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2005-06">2005-06</date><biblScope unit="volume">111</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="353">353</biblScope><biblScope unit="page" to="359">359</biblScope></imprint><idno type="ISSN">0001-6314</idno></series><idno type="istex">0FD63F89D24DADE7DC9BBB31FA0D5FFBB07E52F8</idno><idno type="DOI">10.1111/j.1600-0404.2005.00411.x</idno><idno type="ArticleID">ANE411</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-6314</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer's disease</term><term>Parkinson's disease</term><term>clinical phenotype</term><term>neuropathology</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objectives – Patients with clinical and pathological diagnosis of Parkinson's disease (PD) may, at death, also be found to have the pathological changes of Alzheimer's disease (AD). With this study we aim to determine the influence of AD pathology on the clinical phenotype of PD. Methods – We studied 64 patients who donated their brains to the University of Miami Brain Endowment BankTM and fulfilled the clinical and pathological criteria for PD. For the evaluation of AD pathology we used the CERAD criteria. Dementia was diagnosed, in life, also using standard criteria. Case histories were abstracted and reviewed by one investigator (SP) who then made comparisons between patients. Results – Patients with AD pathology (PD–AD) were older both at the time of diagnosis and death. The presence of AD pathology did not seem to influence disease duration in our cohort of PD patients. As expected there was a clear relation between AD pathology and dementia but not all PD–AD patients were demented. Psychosis and depression were also found to be more prevalent in the PD–AD patients. In the comparison between demented and non‐demented PD–AD patients dementia was more likely to appear in patients with PD and definite criteria for AD. Conclusion – Apart from dementia AD pathology seems to be associated with a number of other clinical characteristics of PD.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>S. Papapetropoulos</name><affiliations><json:string>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</json:string></affiliations></json:item><json:item><name>A. Lieberman</name><affiliations><json:string>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</json:string><json:string>National Parkinson Foundation (NPF), Miami, FL, USA</json:string></affiliations></json:item><json:item><name>J. Gonzalez</name><affiliations><json:string>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</json:string></affiliations></json:item><json:item><name>D. C. Mash</name><affiliations><json:string>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>clinical phenotype</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuropathology</value></json:item></subject><articleId><json:string>ANE411</json:string></articleId><language><json:string>eng</json:string></language><abstract>Objectives – Patients with clinical and pathological diagnosis of Parkinson's disease (PD) may, at death, also be found to have the pathological changes of Alzheimer's disease (AD). With this study we aim to determine the influence of AD pathology on the clinical phenotype of PD. 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C.</forename><surname>Mash</surname></persName><affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</affiliation></author></analytic><monogr><title level="j">Acta Neurologica Scandinavica</title><idno type="pISSN">0001-6314</idno><idno type="eISSN">1600-0404</idno><idno type="DOI">10.1111/(ISSN)1600-0404</idno><imprint><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2005-06"></date><biblScope unit="volume">111</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="353">353</biblScope><biblScope unit="page" to="359">359</biblScope></imprint></monogr><idno type="istex">0FD63F89D24DADE7DC9BBB31FA0D5FFBB07E52F8</idno><idno type="DOI">10.1111/j.1600-0404.2005.00411.x</idno><idno type="ArticleID">ANE411</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Objectives – Patients with clinical and pathological diagnosis of Parkinson's disease (PD) may, at death, also be found to have the pathological changes of Alzheimer's disease (AD). With this study we aim to determine the influence of AD pathology on the clinical phenotype of PD. Methods – We studied 64 patients who donated their brains to the University of Miami Brain Endowment BankTM and fulfilled the clinical and pathological criteria for PD. For the evaluation of AD pathology we used the CERAD criteria. Dementia was diagnosed, in life, also using standard criteria. Case histories were abstracted and reviewed by one investigator (SP) who then made comparisons between patients. Results – Patients with AD pathology (PD–AD) were older both at the time of diagnosis and death. The presence of AD pathology did not seem to influence disease duration in our cohort of PD patients. As expected there was a clear relation between AD pathology and dementia but not all PD–AD patients were demented. Psychosis and depression were also found to be more prevalent in the PD–AD patients. In the comparison between demented and non‐demented PD–AD patients dementia was more likely to appear in patients with PD and definite criteria for AD. Conclusion – Apart from dementia AD pathology seems to be associated with a number of other clinical characteristics of PD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>Alzheimer's disease</term></item><item><term>clinical phenotype</term></item><item><term>neuropathology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-06">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/0FD63F89D24DADE7DC9BBB31FA0D5FFBB07E52F8/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>Munksgaard International Publishers</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-0404</doi><issn type="print">0001-6314</issn><issn type="electronic">1600-0404</issn><idGroup><id type="product" value="ANE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ACTA NEUROLOGICA SCANDINAVICA">Acta Neurologica Scandinavica</title></titleGroup></publicationMeta><publicationMeta level="part" position="06006"><doi origin="wiley">10.1111/ane.2005.111.issue-6</doi><numberingGroup><numbering type="journalVolume" number="111">111</numbering><numbering type="journalIssue" number="6">6</numbering></numberingGroup><coverDate startDate="2005-06">June 2005</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="3" status="forIssue"><doi origin="wiley">10.1111/j.1600-0404.2005.00411.x</doi><idGroup><id type="unit" value="ANE411"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1"><i>Original articles</i></title></titleGroup><eventGroup><event type="firstOnline" date="2005-05-05"></event><event type="publishedOnlineFinalForm" date="2005-05-05"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-15"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="353">353</numbering><numbering type="pageLast" number="359">359</numbering></numberingGroup><correspondenceTo>Papapetropoulos Spiridon, Department of Neurology, School of Medicine, University of Miami, Room 4004, 1501 NW 9th Avenue, 33136 Miami, FL, USA
Tel.: +1 305 243 8461
Fax: +1 305 243 3649
e‐mail: <email>spapapetropoulos@med.miami.edu</email> (or) <email>spyrpap@hotmail.com</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANE.ANE411.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication January 17, 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="7"></count></countGroup><titleGroup><title type="main">Can Alzheimer's type pathology influence the clinical phenotype of Parkinson's disease?</title><title type="shortAuthors"><b>Papapetropoulos et al.</b></title><title type="short"><b>The effect of Alzheimer's type pathology on PD</b></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>S.</givenNames><familyName>Papapetropoulos</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1 #a2"><personName><givenNames>A.</givenNames><familyName>Lieberman</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>J.</givenNames><familyName>Gonzalez</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>D. C.</givenNames><familyName>Mash</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>National Parkinson Foundation (NPF), Miami, FL, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Parkinson's disease</keyword><keyword xml:id="k2">Alzheimer's disease</keyword><keyword xml:id="k3">clinical phenotype</keyword><keyword xml:id="k4">neuropathology</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><!-- Papapetropoulos S, Lieberman A, Gonzalez J, Mash DC. Can Alzheimer's type pathology influence the clinical phenotype of Parkinson's disease?
Acta Neurol Scand 2005: 111: 353–359. © Blackwell Munksgaard 2005. --><p><b>Objectives – </b> Patients with clinical and pathological diagnosis of Parkinson's disease (PD) may, at death, also be found to have the pathological changes of Alzheimer's disease (AD). With this study we aim to determine the influence of AD pathology on the clinical phenotype of PD.</p><p><b>Methods – </b> We studied 64 patients who donated their brains to the University of Miami Brain Endowment Bank<sup>TM</sup> and fulfilled the clinical and pathological criteria for PD. For the evaluation of AD pathology we used the CERAD criteria. Dementia was diagnosed, in life, also using standard criteria. Case histories were abstracted and reviewed by one investigator (SP) who then made comparisons between patients.</p><p><b>Results – </b> Patients with AD pathology (PD–AD) were older both at the time of diagnosis and death. The presence of AD pathology did not seem to influence disease duration in our cohort of PD patients. As expected there was a clear relation between AD pathology and dementia but not all PD–AD patients were demented. Psychosis and depression were also found to be more prevalent in the PD–AD patients. In the comparison between demented and non‐demented PD–AD patients dementia was more likely to appear in patients with PD and definite criteria for AD.</p><p><b>Conclusion – </b> Apart from dementia AD pathology seems to be associated with a number of other clinical characteristics of PD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Can Alzheimer's type pathology influence the clinical phenotype of Parkinson's disease?</title></titleInfo><titleInfo type="abbreviated"><title>The effect of Alzheimer's type pathology on PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Can Alzheimer's type pathology influence the clinical phenotype of Parkinson's disease?</title></titleInfo><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Papapetropoulos</namePart><affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Lieberman</namePart><affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</affiliation><affiliation>National Parkinson Foundation (NPF), Miami, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Gonzalez</namePart><affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D. C.</namePart><namePart type="family">Mash</namePart><affiliation>Department of Neurology, School of Medicine, University of Miami, Miami, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Munksgaard International Publishers</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2005-06</dateIssued><edition>Accepted for publication January 17, 2005</edition><copyrightDate encoding="w3cdtf">2005</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">1</extent><extent unit="tables">7</extent></physicalDescription><abstract lang="en">Objectives – Patients with clinical and pathological diagnosis of Parkinson's disease (PD) may, at death, also be found to have the pathological changes of Alzheimer's disease (AD). With this study we aim to determine the influence of AD pathology on the clinical phenotype of PD. Methods – We studied 64 patients who donated their brains to the University of Miami Brain Endowment BankTM and fulfilled the clinical and pathological criteria for PD. For the evaluation of AD pathology we used the CERAD criteria. Dementia was diagnosed, in life, also using standard criteria. Case histories were abstracted and reviewed by one investigator (SP) who then made comparisons between patients. Results – Patients with AD pathology (PD–AD) were older both at the time of diagnosis and death. The presence of AD pathology did not seem to influence disease duration in our cohort of PD patients. As expected there was a clear relation between AD pathology and dementia but not all PD–AD patients were demented. Psychosis and depression were also found to be more prevalent in the PD–AD patients. In the comparison between demented and non‐demented PD–AD patients dementia was more likely to appear in patients with PD and definite criteria for AD. Conclusion – Apart from dementia AD pathology seems to be associated with a number of other clinical characteristics of PD.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>Alzheimer's disease</topic><topic>clinical phenotype</topic><topic>neuropathology</topic></subject><relatedItem type="host"><titleInfo><title>Acta Neurologica Scandinavica</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0001-6314</identifier><identifier type="eISSN">1600-0404</identifier><identifier type="DOI">10.1111/(ISSN)1600-0404</identifier><identifier type="PublisherID">ANE</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>111</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>353</start><end>359</end><total>7</total></extent></part></relatedItem><identifier type="istex">0FD63F89D24DADE7DC9BBB31FA0D5FFBB07E52F8</identifier><identifier type="DOI">10.1111/j.1600-0404.2005.00411.x</identifier><identifier type="ArticleID">ANE411</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Munksgaard International Publishers</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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