Deprenyl's effect at slowing progression of parkinsonian disability: the DATATOP study
Identifieur interne : 000335 ( Main/Corpus ); précédent : 000334; suivant : 000336Deprenyl's effect at slowing progression of parkinsonian disability: the DATATOP study
Auteurs : P. A. LewittSource :
- Acta Neurologica Scandinavica [ 0001-6314 ] ; 1991-10.
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Abstract
Studying a cohort of 800 mildly‐affected parkinsonians, the North American DATATOP* project has concluded that progression in disability can be attenuated by the use of deprenyl, 10 mg/day. Interim results of this controlled clinical trial were reported after participants received treatment for an average of 12 months. The study found that deprenyl treatment almost halved the risk of reaching a stage of Parkinsonism at which the start of levodopa treatment becomes imperative for lessening disability. In addition to this study end‐point, other ratings supported an improved clinical outcome from the chronic deprenyl (DP) regimen. The 34 investigators conducted clinical evaluations both while subjects received medication and after a 4‐week wash‐out. Though some subjects experienced mild symptomatic improvements of Parkinsonism from DP, these effects were insufficient to account for the DP‐treated group's delay at reaching the study end‐point. In addition to DP, this placebo‐controlled double‐blind study also assessed the possibility of protective effects from another antioxidative strategy, a 2,000 I. U./day regimen of alpha‐tocopherol. To date, results of the latter trial have not been reported. Monoamine oxidase type‐B (MAO‐B) metabolism of dopamine generates hydrogen peroxide and, thereby, an oxidative stress on the nigrostriatal dopaminergic neuron. The inhibition of MAO‐B by DP may have been the means by which progression of Parkinsonism was attenuated, although other mechanisms are also tenable. DATATOP has pointed to the potential for arresting the progression of Parkinson's disease, and has provided an unparalleled opportunity to study the clinical course and neurochemical indices of untreated Parkinsonism. Whether DP's effects are enacted entirely through inhibition of MAO‐B is the theme of a trial similar to DATATOP planned for comparative analysis of another selective MAO‐B inhibitor. *DATATOP: “Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism”.
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DOI: 10.1111/j.1600-0404.1991.tb05025.x
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Lewitt</name><affiliation><mods:affiliation>The Parkinson Study Group</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>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1991-10">1991-10</date><biblScope unit="volume">84</biblScope><biblScope unit="issue">S136</biblScope><biblScope unit="page" from="79">79</biblScope><biblScope unit="page" to="86">86</biblScope></imprint><idno type="ISSN">0001-6314</idno></series><idno type="istex">DEAC0F9C39E60CE9EA6A71C303F8AF99F3A98E12</idno><idno type="DOI">10.1111/j.1600-0404.1991.tb05025.x</idno><idno type="ArticleID">ANE79</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-6314</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>anti‐oxidant therapy</term><term>controlled clinical trial</term><term>deprenyl</term><term>monoamine oxidase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Studying a cohort of 800 mildly‐affected parkinsonians, the North American DATATOP* project has concluded that progression in disability can be attenuated by the use of deprenyl, 10 mg/day. Interim results of this controlled clinical trial were reported after participants received treatment for an average of 12 months. The study found that deprenyl treatment almost halved the risk of reaching a stage of Parkinsonism at which the start of levodopa treatment becomes imperative for lessening disability. In addition to this study end‐point, other ratings supported an improved clinical outcome from the chronic deprenyl (DP) regimen. The 34 investigators conducted clinical evaluations both while subjects received medication and after a 4‐week wash‐out. Though some subjects experienced mild symptomatic improvements of Parkinsonism from DP, these effects were insufficient to account for the DP‐treated group's delay at reaching the study end‐point. In addition to DP, this placebo‐controlled double‐blind study also assessed the possibility of protective effects from another antioxidative strategy, a 2,000 I. U./day regimen of alpha‐tocopherol. To date, results of the latter trial have not been reported. Monoamine oxidase type‐B (MAO‐B) metabolism of dopamine generates hydrogen peroxide and, thereby, an oxidative stress on the nigrostriatal dopaminergic neuron. The inhibition of MAO‐B by DP may have been the means by which progression of Parkinsonism was attenuated, although other mechanisms are also tenable. DATATOP has pointed to the potential for arresting the progression of Parkinson's disease, and has provided an unparalleled opportunity to study the clinical course and neurochemical indices of untreated Parkinsonism. Whether DP's effects are enacted entirely through inhibition of MAO‐B is the theme of a trial similar to DATATOP planned for comparative analysis of another selective MAO‐B inhibitor. *DATATOP: “Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism”.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>P. A. 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Interim results of this controlled clinical trial were reported after participants received treatment for an average of 12 months. The study found that deprenyl treatment almost halved the risk of reaching a stage of Parkinsonism at which the start of levodopa treatment becomes imperative for lessening disability. In addition to this study end‐point, other ratings supported an improved clinical outcome from the chronic deprenyl (DP) regimen. The 34 investigators conducted clinical evaluations both while subjects received medication and after a 4‐week wash‐out. Though some subjects experienced mild symptomatic improvements of Parkinsonism from DP, these effects were insufficient to account for the DP‐treated group's delay at reaching the study end‐point. In addition to DP, this placebo‐controlled double‐blind study also assessed the possibility of protective effects from another antioxidative strategy, a 2,000 I. U./day regimen of alpha‐tocopherol. To date, results of the latter trial have not been reported. Monoamine oxidase type‐B (MAO‐B) metabolism of dopamine generates hydrogen peroxide and, thereby, an oxidative stress on the nigrostriatal dopaminergic neuron. The inhibition of MAO‐B by DP may have been the means by which progression of Parkinsonism was attenuated, although other mechanisms are also tenable. DATATOP has pointed to the potential for arresting the progression of Parkinson's disease, and has provided an unparalleled opportunity to study the clinical course and neurochemical indices of untreated Parkinsonism. 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A.</forename><surname>LeWitt</surname></persName><note type="correspondence"><p>Correspondence: Department of Neurology, Wayne State University School of Medicine, 14800 West McNichols, Suite 001 Detroit, Michigan 48235 USA</p></note><affiliation>The Parkinson Study Group</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>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1991-10"></date><biblScope unit="volume">84</biblScope><biblScope unit="issue">S136</biblScope><biblScope unit="page" from="79">79</biblScope><biblScope unit="page" to="86">86</biblScope></imprint></monogr><idno type="istex">DEAC0F9C39E60CE9EA6A71C303F8AF99F3A98E12</idno><idno type="DOI">10.1111/j.1600-0404.1991.tb05025.x</idno><idno type="ArticleID">ANE79</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1991</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Studying a cohort of 800 mildly‐affected parkinsonians, the North American DATATOP* project has concluded that progression in disability can be attenuated by the use of deprenyl, 10 mg/day. Interim results of this controlled clinical trial were reported after participants received treatment for an average of 12 months. The study found that deprenyl treatment almost halved the risk of reaching a stage of Parkinsonism at which the start of levodopa treatment becomes imperative for lessening disability. In addition to this study end‐point, other ratings supported an improved clinical outcome from the chronic deprenyl (DP) regimen. The 34 investigators conducted clinical evaluations both while subjects received medication and after a 4‐week wash‐out. Though some subjects experienced mild symptomatic improvements of Parkinsonism from DP, these effects were insufficient to account for the DP‐treated group's delay at reaching the study end‐point. In addition to DP, this placebo‐controlled double‐blind study also assessed the possibility of protective effects from another antioxidative strategy, a 2,000 I. U./day regimen of alpha‐tocopherol. To date, results of the latter trial have not been reported. Monoamine oxidase type‐B (MAO‐B) metabolism of dopamine generates hydrogen peroxide and, thereby, an oxidative stress on the nigrostriatal dopaminergic neuron. The inhibition of MAO‐B by DP may have been the means by which progression of Parkinsonism was attenuated, although other mechanisms are also tenable. DATATOP has pointed to the potential for arresting the progression of Parkinson's disease, and has provided an unparalleled opportunity to study the clinical course and neurochemical indices of untreated Parkinsonism. Whether DP's effects are enacted entirely through inhibition of MAO‐B is the theme of a trial similar to DATATOP planned for comparative analysis of another selective MAO‐B inhibitor. *DATATOP: “Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism”.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>deprenyl</term></item><item><term>monoamine oxidase</term></item><item><term>controlled clinical trial</term></item><item><term>anti‐oxidant therapy</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1991-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/DEAC0F9C39E60CE9EA6A71C303F8AF99F3A98E12/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>Blackwell Publishing Ltd</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="10000"><doi origin="wiley">10.1111/ane.1991.84.issue-S136</doi><numberingGroup><numbering type="journalVolume" number="84">84</numbering><numbering type="journalIssue">S136</numbering></numberingGroup><coverDate startDate="1991-10">October 1991</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0007900" status="forIssue"><doi origin="wiley">10.1111/j.1600-0404.1991.tb05025.x</doi><idGroup><id type="unit" value="ANE79"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="tocHeading1">Original article</title></titleGroup><copyright>1991 Blackwell Munksgaard</copyright><eventGroup><event type="firstOnline" date="2009-01-29"></event><event type="publishedOnlineFinalForm" date="2009-01-29"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.6 mode:FullText source:HeaderRef result:HeaderRef" date="2010-04-20"></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="79">79</numbering><numbering type="pageLast" number="86">86</numbering></numberingGroup><correspondenceTo>Department of Neurology, Wayne State University School of Medicine, 14800 West McNichols, Suite 001 Detroit, Michigan 48235 USA</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANE.ANE79.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="referenceTotal" number="25"></count><count type="linksCrossRef" number="2"></count></countGroup><titleGroup><title type="main">Deprenyl's effect at slowing progression of parkinsonian disability: the DATATOP study</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>P. 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The study found that deprenyl treatment almost halved the risk of reaching a stage of Parkinsonism at which the start of levodopa treatment becomes imperative for lessening disability. In addition to this study end‐point, other ratings supported an improved clinical outcome from the chronic deprenyl (DP) regimen. The 34 investigators conducted clinical evaluations both while subjects received medication and after a 4‐week wash‐out. Though some subjects experienced mild symptomatic improvements of Parkinsonism from DP, these effects were insufficient to account for the DP‐treated group's delay at reaching the study end‐point. In addition to DP, this placebo‐controlled double‐blind study also assessed the possibility of protective effects from another antioxidative strategy, a 2,000 I. U./day regimen of alpha‐tocopherol. To date, results of the latter trial have not been reported.</p><p>Monoamine oxidase type‐B (MAO‐B) metabolism of dopamine generates hydrogen peroxide and, thereby, an oxidative stress on the nigrostriatal dopaminergic neuron. The inhibition of MAO‐B by DP may have been the means by which progression of Parkinsonism was attenuated, although other mechanisms are also tenable. DATATOP has pointed to the potential for arresting the progression of Parkinson's disease, and has provided an unparalleled opportunity to study the clinical course and neurochemical indices of untreated Parkinsonism. Whether DP's effects are enacted entirely through inhibition of MAO‐B is the theme of a trial similar to DATATOP planned for comparative analysis of another selective MAO‐B inhibitor.</p><p>*DATATOP: “Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism”.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Deprenyl's effect at slowing progression of parkinsonian disability: the DATATOP study</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Deprenyl's effect at slowing progression of parkinsonian disability: the DATATOP study</title></titleInfo><name type="personal"><namePart type="given">P. A.</namePart><namePart type="family">LeWitt</namePart><affiliation>The Parkinson Study Group</affiliation><description>Correspondence: Department of Neurology, Wayne State University School of Medicine, 14800 West McNichols, Suite 001 Detroit, Michigan 48235 USA</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1991-10</dateIssued><copyrightDate encoding="w3cdtf">1991</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="references">25</extent></physicalDescription><abstract lang="en">Studying a cohort of 800 mildly‐affected parkinsonians, the North American DATATOP* project has concluded that progression in disability can be attenuated by the use of deprenyl, 10 mg/day. Interim results of this controlled clinical trial were reported after participants received treatment for an average of 12 months. The study found that deprenyl treatment almost halved the risk of reaching a stage of Parkinsonism at which the start of levodopa treatment becomes imperative for lessening disability. In addition to this study end‐point, other ratings supported an improved clinical outcome from the chronic deprenyl (DP) regimen. The 34 investigators conducted clinical evaluations both while subjects received medication and after a 4‐week wash‐out. Though some subjects experienced mild symptomatic improvements of Parkinsonism from DP, these effects were insufficient to account for the DP‐treated group's delay at reaching the study end‐point. In addition to DP, this placebo‐controlled double‐blind study also assessed the possibility of protective effects from another antioxidative strategy, a 2,000 I. U./day regimen of alpha‐tocopherol. To date, results of the latter trial have not been reported. Monoamine oxidase type‐B (MAO‐B) metabolism of dopamine generates hydrogen peroxide and, thereby, an oxidative stress on the nigrostriatal dopaminergic neuron. The inhibition of MAO‐B by DP may have been the means by which progression of Parkinsonism was attenuated, although other mechanisms are also tenable. DATATOP has pointed to the potential for arresting the progression of Parkinson's disease, and has provided an unparalleled opportunity to study the clinical course and neurochemical indices of untreated Parkinsonism. Whether DP's effects are enacted entirely through inhibition of MAO‐B is the theme of a trial similar to DATATOP planned for comparative analysis of another selective MAO‐B inhibitor. *DATATOP: “Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism”.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>deprenyl</topic><topic>monoamine oxidase</topic><topic>controlled clinical trial</topic><topic>anti‐oxidant therapy</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>1991</date><detail type="volume"><caption>vol.</caption><number>84</number></detail><detail type="issue"><caption>no.</caption><number>S136</number></detail><extent unit="pages"><start>79</start><end>86</end><total>8</total></extent></part></relatedItem><identifier type="istex">DEAC0F9C39E60CE9EA6A71C303F8AF99F3A98E12</identifier><identifier type="DOI">10.1111/j.1600-0404.1991.tb05025.x</identifier><identifier type="ArticleID">ANE79</identifier><accessCondition type="use and reproduction" contentType="copyright">1991 Blackwell Munksgaard</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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