Association between amantadine and the onset of dementia in Parkinson's disease
Identifieur interne : 001352 ( Istex/Corpus ); précédent : 001351; suivant : 001353Association between amantadine and the onset of dementia in Parkinson's disease
Auteurs : Rivka Inzelberg ; Ubaldo Bonuccelli ; Edna Schechtman ; Ala Miniowich ; Rosa Strugatsky ; Roberto Ceravolo ; Chiara Logi ; Carlo Rossi ; Colin Klein ; J. Martin RabeySource :
- Movement Disorders [ 0885-3185 ] ; 2006-09.
English descriptors
- KwdEn :
Abstract
The objective of this study is to compare the occurrence of dementia among Parkinson's disease (PD) patients treated with amantadine (AM group) with those never exposed to it (NoAM group). PD dementia shares neuroanatomical and biochemical similarities with Alzheimer's disease (AD). Memantine, an N‐methyl‐D‐aspartate (NMDA) receptor antagonist has been shown to be beneficial in AD. Memantine is a dimethyl derivative of amantadine, which also possesses NMDA receptor blocking properties. We hypothesized that amantadine could have a beneficial effect on the occurrence of PD dementia. PD patients attending the Movement Disorders Clinics in Hillel Yaffe, Asaf Harofe Medical Centers (Israel) and Pisa (Italy) were included. Taking the onset of dementia as the endpoint, survival curves for AM and NoAM patients were estimated by the Kaplan–Meier method. The study population consisted of 593 patients (age, 69.5 ± 9.9 years; PD duration, 9.2 ± 6.0 years; 263 patients (44%) amantadine treated). The endpoint of dementia was reached by 116 patients (20%). PD duration until dementia was significantly longer for AM patients (9.1 ± 5.7 years) than for NoAM patients (5.9 ± 4.6 years, P = 0.006). The duration of amantadine exposure positively correlated with PD duration until dementia (P = 0.0001). Survival analysis, taking dementia onset as endpoint, showed slower mental decline in AM patients (Log rank P = 0.0049, Wilcoxon P = 0.0024). Mini‐Mental State Examination scores were significantly higher for AM patients than for the NoAM group (P = 0.01). Age of PD onset also significantly influenced the duration of PD until dementia. Amantadine use may delay the onset of dementia in PD patients and may attenuate its severity. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.20968
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ISTEX:AEBB6144CDA4BCBA8F00BF9EDBF063AD31C40036Le document en format XML
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Martin" last="Rabey">J. Martin Rabey</name><affiliation><mods:affiliation>Department of Neurology, Asaf Harofe Medical Center, Tzrifin and Sackler Faculty of Medicine, Tel‐Aviv University, Ramat Aviv, Israel</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="2006-09">2006-09</date><biblScope unit="vol">21</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1375">1375</biblScope><biblScope unit="page" to="1379">1379</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">AEBB6144CDA4BCBA8F00BF9EDBF063AD31C40036</idno><idno type="DOI">10.1002/mds.20968</idno><idno type="ArticleID">MDS20968</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>amantadine</term><term>dementia</term><term>selegiline</term><term>therapy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The objective of this study is to compare the occurrence of dementia among Parkinson's disease (PD) patients treated with amantadine (AM group) with those never exposed to it (NoAM group). PD dementia shares neuroanatomical and biochemical similarities with Alzheimer's disease (AD). Memantine, an N‐methyl‐D‐aspartate (NMDA) receptor antagonist has been shown to be beneficial in AD. Memantine is a dimethyl derivative of amantadine, which also possesses NMDA receptor blocking properties. We hypothesized that amantadine could have a beneficial effect on the occurrence of PD dementia. PD patients attending the Movement Disorders Clinics in Hillel Yaffe, Asaf Harofe Medical Centers (Israel) and Pisa (Italy) were included. Taking the onset of dementia as the endpoint, survival curves for AM and NoAM patients were estimated by the Kaplan–Meier method. The study population consisted of 593 patients (age, 69.5 ± 9.9 years; PD duration, 9.2 ± 6.0 years; 263 patients (44%) amantadine treated). The endpoint of dementia was reached by 116 patients (20%). PD duration until dementia was significantly longer for AM patients (9.1 ± 5.7 years) than for NoAM patients (5.9 ± 4.6 years, P = 0.006). The duration of amantadine exposure positively correlated with PD duration until dementia (P = 0.0001). Survival analysis, taking dementia onset as endpoint, showed slower mental decline in AM patients (Log rank P = 0.0049, Wilcoxon P = 0.0024). Mini‐Mental State Examination scores were significantly higher for AM patients than for the NoAM group (P = 0.01). Age of PD onset also significantly influenced the duration of PD until dementia. Amantadine use may delay the onset of dementia in PD patients and may attenuate its severity. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Rivka Inzelberg MD</name><affiliations><json:string>Department of Neurology, Hillel Yaffe Medical Center, Hadera, Israel</json:string><json:string>Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel</json:string></affiliations></json:item><json:item><name>Ubaldo Bonuccelli MD</name><affiliations><json:string>Department of Neurosciences, University of Pisa, Italy</json:string></affiliations></json:item><json:item><name>Edna Schechtman PhD</name><affiliations><json:string>Department of Industrial Engineering and Management, Ben Gurion University, Beer Sheva, Israel</json:string></affiliations></json:item><json:item><name>Ala Miniowich MD</name><affiliations><json:string>Department of Neurology, Asaf Harofe Medical Center, Tzrifin and Sackler Faculty of Medicine, Tel‐Aviv University, Ramat Aviv, Israel</json:string></affiliations></json:item><json:item><name>Rosa Strugatsky MD</name><affiliations><json:string>Department of Neurology, Hillel Yaffe Medical Center, Hadera, Israel</json:string></affiliations></json:item><json:item><name>Roberto Ceravolo MD</name><affiliations><json:string>Department of Neurosciences, University of Pisa, Italy</json:string></affiliations></json:item><json:item><name>Chiara Logi MD</name><affiliations><json:string>Department of Neurosciences, University of Pisa, Italy</json:string></affiliations></json:item><json:item><name>Carlo Rossi MD</name><affiliations><json:string>Department of Neurosciences, University of Pisa, Italy</json:string></affiliations></json:item><json:item><name>Colin Klein MD</name><affiliations><json:string>Department of Neurology, Asaf Harofe Medical Center, Tzrifin and Sackler Faculty of Medicine, Tel‐Aviv University, Ramat Aviv, Israel</json:string></affiliations></json:item><json:item><name>J. Martin Rabey MD</name><affiliations><json:string>Department of Neurology, Asaf Harofe Medical Center, Tzrifin and Sackler Faculty of Medicine, Tel‐Aviv University, Ramat Aviv, Israel</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>dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>therapy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>amantadine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>selegiline</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The objective of this study is to compare the occurrence of dementia among Parkinson's disease (PD) patients treated with amantadine (AM group) with those never exposed to it (NoAM group). PD dementia shares neuroanatomical and biochemical similarities with Alzheimer's disease (AD). Memantine, an N‐methyl‐D‐aspartate (NMDA) receptor antagonist has been shown to be beneficial in AD. Memantine is a dimethyl derivative of amantadine, which also possesses NMDA receptor blocking properties. We hypothesized that amantadine could have a beneficial effect on the occurrence of PD dementia. PD patients attending the Movement Disorders Clinics in Hillel Yaffe, Asaf Harofe Medical Centers (Israel) and Pisa (Italy) were included. Taking the onset of dementia as the endpoint, survival curves for AM and NoAM patients were estimated by the Kaplan–Meier method. The study population consisted of 593 patients (age, 69.5 ± 9.9 years; PD duration, 9.2 ± 6.0 years; 263 patients (44%) amantadine treated). The endpoint of dementia was reached by 116 patients (20%). PD duration until dementia was significantly longer for AM patients (9.1 ± 5.7 years) than for NoAM patients (5.9 ± 4.6 years, P = 0.006). The duration of amantadine exposure positively correlated with PD duration until dementia (P = 0.0001). Survival analysis, taking dementia onset as endpoint, showed slower mental decline in AM patients (Log rank P = 0.0049, Wilcoxon P = 0.0024). Mini‐Mental State Examination scores were significantly higher for AM patients than for the NoAM group (P = 0.01). Age of PD onset also significantly influenced the duration of PD until dementia. 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Martin</forename><surname>Rabey</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, Asaf Harofe Medical Center, Tzrifin and Sackler Faculty of Medicine, Tel‐Aviv University, Ramat Aviv, Israel</affiliation></author></analytic><monogr><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="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-09"></date><biblScope unit="vol">21</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1375">1375</biblScope><biblScope unit="page" to="1379">1379</biblScope></imprint></monogr><idno type="istex">AEBB6144CDA4BCBA8F00BF9EDBF063AD31C40036</idno><idno type="DOI">10.1002/mds.20968</idno><idno type="ArticleID">MDS20968</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The objective of this study is to compare the occurrence of dementia among Parkinson's disease (PD) patients treated with amantadine (AM group) with those never exposed to it (NoAM group). PD dementia shares neuroanatomical and biochemical similarities with Alzheimer's disease (AD). Memantine, an N‐methyl‐D‐aspartate (NMDA) receptor antagonist has been shown to be beneficial in AD. Memantine is a dimethyl derivative of amantadine, which also possesses NMDA receptor blocking properties. We hypothesized that amantadine could have a beneficial effect on the occurrence of PD dementia. PD patients attending the Movement Disorders Clinics in Hillel Yaffe, Asaf Harofe Medical Centers (Israel) and Pisa (Italy) were included. Taking the onset of dementia as the endpoint, survival curves for AM and NoAM patients were estimated by the Kaplan–Meier method. The study population consisted of 593 patients (age, 69.5 ± 9.9 years; PD duration, 9.2 ± 6.0 years; 263 patients (44%) amantadine treated). The endpoint of dementia was reached by 116 patients (20%). PD duration until dementia was significantly longer for AM patients (9.1 ± 5.7 years) than for NoAM patients (5.9 ± 4.6 years, P = 0.006). The duration of amantadine exposure positively correlated with PD duration until dementia (P = 0.0001). Survival analysis, taking dementia onset as endpoint, showed slower mental decline in AM patients (Log rank P = 0.0049, Wilcoxon P = 0.0024). Mini‐Mental State Examination scores were significantly higher for AM patients than for the NoAM group (P = 0.01). Age of PD onset also significantly influenced the duration of PD until dementia. Amantadine use may delay the onset of dementia in PD patients and may attenuate its severity. © 2006 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>dementia</term></item><item><term>therapy</term></item><item><term>amantadine</term></item><item><term>selegiline</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-08-12">Received</change><change when="2006-01-24">Registration</change><change when="2006-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/AEBB6144CDA4BCBA8F00BF9EDBF063AD31C40036/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. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="90"><doi origin="wiley" registered="yes">10.1002/mds.v21:9</doi><numberingGroup><numbering type="journalVolume" number="21">21</numbering><numbering type="journalIssue">9</numbering></numberingGroup><coverDate startDate="2006-09">September 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="120" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.20968</doi><idGroup><id type="unit" value="MDS20968"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2006 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2005-08-12"></event><event type="manuscriptRevised" date="2006-01-24"></event><event type="manuscriptAccepted" date="2006-01-24"></event><event type="publishedOnlineEarlyUnpaginated" date="2006-05-16"></event><event type="firstOnline" date="2006-05-16"></event><event type="publishedOnlineFinalForm" date="2006-09-20"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.6 mode:FullText source:FullText result:FullText" date="2010-04-21"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">1375</numbering><numbering type="pageLast">1379</numbering></numberingGroup><correspondenceTo>Department of Neurology, Hillel Yaffe Medical Center, Hadera, 38100, Israel</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS20968.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="38"></count><count type="wordTotal" number="3768"></count></countGroup><titleGroup><title type="main" xml:lang="en">Association between amantadine and the onset of dementia in Parkinson's disease</title><title type="short" xml:lang="en">Amantadine and Dementia Onset PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Rivka</givenNames><familyName>Inzelberg</familyName><degrees>MD</degrees></personName><contactDetails><email>irivka@tx.technion.ac.il</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Ubaldo</givenNames><familyName>Bonuccelli</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Edna</givenNames><familyName>Schechtman</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Ala</givenNames><familyName>Miniowich</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Rosa</givenNames><familyName>Strugatsky</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Roberto</givenNames><familyName>Ceravolo</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Chiara</givenNames><familyName>Logi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Carlo</givenNames><familyName>Rossi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Colin</givenNames><familyName>Klein</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af5"><personName><givenNames>J. Martin</givenNames><familyName>Rabey</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IL" type="organization"><unparsedAffiliation>Department of Neurology, Hillel Yaffe Medical Center, Hadera, Israel</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="IL" type="organization"><unparsedAffiliation>Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="IT" type="organization"><unparsedAffiliation>Department of Neurosciences, University of Pisa, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="IL" type="organization"><unparsedAffiliation>Department of Industrial Engineering and Management, Ben Gurion University, Beer Sheva, Israel</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="IL" type="organization"><unparsedAffiliation>Department of Neurology, Asaf Harofe Medical Center, Tzrifin and Sackler Faculty of Medicine, Tel‐Aviv University, Ramat Aviv, Israel</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">dementia</keyword><keyword xml:id="kwd3">therapy</keyword><keyword xml:id="kwd4">amantadine</keyword><keyword xml:id="kwd5">selegiline</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The objective of this study is to compare the occurrence of dementia among Parkinson's disease (PD) patients treated with amantadine (AM group) with those never exposed to it (NoAM group). PD dementia shares neuroanatomical and biochemical similarities with Alzheimer's disease (AD). Memantine, an <i>N</i>‐methyl‐<sc>D</sc>‐aspartate (NMDA) receptor antagonist has been shown to be beneficial in AD. Memantine is a dimethyl derivative of amantadine, which also possesses NMDA receptor blocking properties. We hypothesized that amantadine could have a beneficial effect on the occurrence of PD dementia. PD patients attending the Movement Disorders Clinics in Hillel Yaffe, Asaf Harofe Medical Centers (Israel) and Pisa (Italy) were included. Taking the onset of dementia as the endpoint, survival curves for AM and NoAM patients were estimated by the Kaplan–Meier method. The study population consisted of 593 patients (age, 69.5 ± 9.9 years; PD duration, 9.2 ± 6.0 years; 263 patients (44%) amantadine treated). The endpoint of dementia was reached by 116 patients (20%). PD duration until dementia was significantly longer for AM patients (9.1 ± 5.7 years) than for NoAM patients (5.9 ± 4.6 years, <i>P</i> = 0.006). The duration of amantadine exposure positively correlated with PD duration until dementia (<i>P</i> = 0.0001). Survival analysis, taking dementia onset as endpoint, showed slower mental decline in AM patients (Log rank <i>P</i> = 0.0049, Wilcoxon <i>P</i> = 0.0024). Mini‐Mental State Examination scores were significantly higher for AM patients than for the NoAM group (<i>P</i> = 0.01). Age of PD onset also significantly influenced the duration of PD until dementia. Amantadine use may delay the onset of dementia in PD patients and may attenuate its severity. © 2006 Movement Disorder Society</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>Association between amantadine and the onset of dementia in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Amantadine and Dementia Onset PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Association between amantadine and the onset of dementia in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Rivka</namePart><namePart type="family">Inzelberg</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Hillel Yaffe Medical Center, Hadera, Israel</affiliation><affiliation>Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel</affiliation><description>Correspondence: Department of Neurology, Hillel Yaffe Medical Center, Hadera, 38100, Israel</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ubaldo</namePart><namePart type="family">Bonuccelli</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurosciences, University of Pisa, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Edna</namePart><namePart type="family">Schechtman</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Industrial Engineering and Management, Ben Gurion University, Beer Sheva, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ala</namePart><namePart type="family">Miniowich</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Asaf Harofe Medical Center, Tzrifin and Sackler Faculty of Medicine, Tel‐Aviv University, Ramat Aviv, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rosa</namePart><namePart type="family">Strugatsky</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Hillel Yaffe Medical Center, Hadera, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roberto</namePart><namePart type="family">Ceravolo</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurosciences, University of Pisa, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chiara</namePart><namePart type="family">Logi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurosciences, University of Pisa, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carlo</namePart><namePart type="family">Rossi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurosciences, University of Pisa, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Colin</namePart><namePart type="family">Klein</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Asaf Harofe Medical Center, Tzrifin and Sackler Faculty of Medicine, Tel‐Aviv University, Ramat Aviv, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. Martin</namePart><namePart type="family">Rabey</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Asaf Harofe Medical Center, Tzrifin and Sackler Faculty of Medicine, Tel‐Aviv University, Ramat Aviv, Israel</affiliation><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">2006-09</dateIssued><dateCaptured encoding="w3cdtf">2005-08-12</dateCaptured><dateValid encoding="w3cdtf">2006-01-24</dateValid><copyrightDate encoding="w3cdtf">2006</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">2</extent><extent unit="references">38</extent><extent unit="words">3768</extent></physicalDescription><abstract lang="en">The objective of this study is to compare the occurrence of dementia among Parkinson's disease (PD) patients treated with amantadine (AM group) with those never exposed to it (NoAM group). PD dementia shares neuroanatomical and biochemical similarities with Alzheimer's disease (AD). Memantine, an N‐methyl‐D‐aspartate (NMDA) receptor antagonist has been shown to be beneficial in AD. Memantine is a dimethyl derivative of amantadine, which also possesses NMDA receptor blocking properties. We hypothesized that amantadine could have a beneficial effect on the occurrence of PD dementia. PD patients attending the Movement Disorders Clinics in Hillel Yaffe, Asaf Harofe Medical Centers (Israel) and Pisa (Italy) were included. Taking the onset of dementia as the endpoint, survival curves for AM and NoAM patients were estimated by the Kaplan–Meier method. The study population consisted of 593 patients (age, 69.5 ± 9.9 years; PD duration, 9.2 ± 6.0 years; 263 patients (44%) amantadine treated). The endpoint of dementia was reached by 116 patients (20%). PD duration until dementia was significantly longer for AM patients (9.1 ± 5.7 years) than for NoAM patients (5.9 ± 4.6 years, P = 0.006). The duration of amantadine exposure positively correlated with PD duration until dementia (P = 0.0001). Survival analysis, taking dementia onset as endpoint, showed slower mental decline in AM patients (Log rank P = 0.0049, Wilcoxon P = 0.0024). Mini‐Mental State Examination scores were significantly higher for AM patients than for the NoAM group (P = 0.01). Age of PD onset also significantly influenced the duration of PD until dementia. Amantadine use may delay the onset of dementia in PD patients and may attenuate its severity. © 2006 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>dementia</topic><topic>therapy</topic><topic>amantadine</topic><topic>selegiline</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>Research 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>2006</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>1375</start><end>1379</end><total>5</total></extent></part></relatedItem><identifier type="istex">AEBB6144CDA4BCBA8F00BF9EDBF063AD31C40036</identifier><identifier type="DOI">10.1002/mds.20968</identifier><identifier type="ArticleID">MDS20968</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 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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