Neurotransmission in Parkinson’s disease: beyond dopamine
Identifieur interne : 000278 ( Main/Corpus ); précédent : 000277; suivant : 000279Neurotransmission in Parkinson’s disease: beyond dopamine
Auteurs : P. BaroneSource :
- European Journal of Neurology [ 1351-5101 ] ; 2010-03.
English descriptors
Abstract
Parkinson’s disease (PD) is most frequently associated with characteristic motor symptoms that are known to arise with degeneration of dopaminergic neurons. However, patients with this disease also experience a multitude of non‐motor symptoms, such as sleep disturbances, fatigue, apathy, anxiety, depression, cognitive impairment, dementia, olfactory dysfunction, pain, sweating and constipation, some of which can be at least as debilitating as the movement disorders and have a major impact on patients’ quality of life. Many of these non‐motor symptoms may be evident prior to the onset of motor dysfunction. The neuropathology of PD has shown that complex, interconnected neuronal systems, regulated by a number of different neurotransmitters in addition to dopamine, are involved in the aetiology of motor and non‐motor symptoms. This review focuses on the non‐dopaminergic neurotransmission systems associated with PD with particular reference to the effect that their modulation and interaction with dopamine has on the non‐motor symptoms of the disease. PD treatments that focus on the dopaminergic system alone are unable to alleviate both motor and non‐motor symptoms, particularly those that develop at early stages of the disease. The development of agents that interact with several of the affected neurotransmission systems could prove invaluable for the treatment of this disease.
Url:
DOI: 10.1111/j.1468-1331.2009.02900.x
Links to Exploration step
ISTEX:DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neurotransmission in Parkinson’s disease: beyond dopamine</title><author><name sortKey="Barone, P" sort="Barone, P" uniqKey="Barone P" first="P." last="Barone">P. Barone</name><affiliation><mods:affiliation>Dipartimento di Scienze Neurologiche and IDC‐Hermitage‐Capodimonte, Naples, Italy</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1111/j.1468-1331.2009.02900.x</idno><idno type="url">https://api.istex.fr/document/DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000278</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Neurotransmission in Parkinson’s disease: beyond dopamine</title><author><name sortKey="Barone, P" sort="Barone, P" uniqKey="Barone P" first="P." last="Barone">P. Barone</name><affiliation><mods:affiliation>Dipartimento di Scienze Neurologiche and IDC‐Hermitage‐Capodimonte, Naples, Italy</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neurology</title><idno type="ISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-03">2010-03</date><biblScope unit="volume">17</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="364">364</biblScope><biblScope unit="page" to="376">376</biblScope></imprint><idno type="ISSN">1351-5101</idno></series><idno type="istex">DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99</idno><idno type="DOI">10.1111/j.1468-1331.2009.02900.x</idno><idno type="ArticleID">ENE2900</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1351-5101</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson’s disease</term><term>neurotransmitter</term><term>non‐motor symptoms</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson’s disease (PD) is most frequently associated with characteristic motor symptoms that are known to arise with degeneration of dopaminergic neurons. However, patients with this disease also experience a multitude of non‐motor symptoms, such as sleep disturbances, fatigue, apathy, anxiety, depression, cognitive impairment, dementia, olfactory dysfunction, pain, sweating and constipation, some of which can be at least as debilitating as the movement disorders and have a major impact on patients’ quality of life. Many of these non‐motor symptoms may be evident prior to the onset of motor dysfunction. The neuropathology of PD has shown that complex, interconnected neuronal systems, regulated by a number of different neurotransmitters in addition to dopamine, are involved in the aetiology of motor and non‐motor symptoms. This review focuses on the non‐dopaminergic neurotransmission systems associated with PD with particular reference to the effect that their modulation and interaction with dopamine has on the non‐motor symptoms of the disease. PD treatments that focus on the dopaminergic system alone are unable to alleviate both motor and non‐motor symptoms, particularly those that develop at early stages of the disease. The development of agents that interact with several of the affected neurotransmission systems could prove invaluable for the treatment of this disease.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>P. Barone</name><affiliations><json:string>Dipartimento di Scienze Neurologiche and IDC‐Hermitage‐Capodimonte, Naples, Italy</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>neurotransmitter</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>non‐motor symptoms</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson’s disease</value></json:item></subject><articleId><json:string>ENE2900</json:string></articleId><language><json:string>eng</json:string></language><abstract>Parkinson’s disease (PD) is most frequently associated with characteristic motor symptoms that are known to arise with degeneration of dopaminergic neurons. However, patients with this disease also experience a multitude of non‐motor symptoms, such as sleep disturbances, fatigue, apathy, anxiety, depression, cognitive impairment, dementia, olfactory dysfunction, pain, sweating and constipation, some of which can be at least as debilitating as the movement disorders and have a major impact on patients’ quality of life. Many of these non‐motor symptoms may be evident prior to the onset of motor dysfunction. The neuropathology of PD has shown that complex, interconnected neuronal systems, regulated by a number of different neurotransmitters in addition to dopamine, are involved in the aetiology of motor and non‐motor symptoms. This review focuses on the non‐dopaminergic neurotransmission systems associated with PD with particular reference to the effect that their modulation and interaction with dopamine has on the non‐motor symptoms of the disease. PD treatments that focus on the dopaminergic system alone are unable to alleviate both motor and non‐motor symptoms, particularly those that develop at early stages of the disease. The development of agents that interact with several of the affected neurotransmission systems could prove invaluable for the treatment of this disease.</abstract><qualityIndicators><score>7.424</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>3</keywordCount><abstractCharCount>1396</abstractCharCount><pdfWordCount>7888</pdfWordCount><pdfCharCount>54987</pdfCharCount><pdfPageCount>13</pdfPageCount><abstractWordCount>202</abstractWordCount></qualityIndicators><title>Neurotransmission in Parkinson’s disease: beyond dopamine</title><genre><json:string>review-article</json:string></genre><host><volume>17</volume><publisherId><json:string>ENE</json:string></publisherId><pages><total>13</total><last>376</last><first>364</first></pages><issn><json:string>1351-5101</json:string></issn><issue>3</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-1331</json:string></eissn><title>European Journal of Neurology</title><doi><json:string>10.1111/(ISSN)1468-1331</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1111/j.1468-1331.2009.02900.x</json:string></doi><id>DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Neurotransmission in Parkinson’s disease: beyond dopamine</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Neurotransmission in Parkinson’s disease: beyond dopamine</title><author><persName><forename type="first">P.</forename><surname>Barone</surname></persName><affiliation>Dipartimento di Scienze Neurologiche and IDC‐Hermitage‐Capodimonte, Naples, Italy</affiliation></author></analytic><monogr><title level="j">European Journal of Neurology</title><idno type="pISSN">1351-5101</idno><idno type="eISSN">1468-1331</idno><idno type="DOI">10.1111/(ISSN)1468-1331</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-03"></date><biblScope unit="volume">17</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="364">364</biblScope><biblScope unit="page" to="376">376</biblScope></imprint></monogr><idno type="istex">DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99</idno><idno type="DOI">10.1111/j.1468-1331.2009.02900.x</idno><idno type="ArticleID">ENE2900</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Parkinson’s disease (PD) is most frequently associated with characteristic motor symptoms that are known to arise with degeneration of dopaminergic neurons. However, patients with this disease also experience a multitude of non‐motor symptoms, such as sleep disturbances, fatigue, apathy, anxiety, depression, cognitive impairment, dementia, olfactory dysfunction, pain, sweating and constipation, some of which can be at least as debilitating as the movement disorders and have a major impact on patients’ quality of life. Many of these non‐motor symptoms may be evident prior to the onset of motor dysfunction. The neuropathology of PD has shown that complex, interconnected neuronal systems, regulated by a number of different neurotransmitters in addition to dopamine, are involved in the aetiology of motor and non‐motor symptoms. This review focuses on the non‐dopaminergic neurotransmission systems associated with PD with particular reference to the effect that their modulation and interaction with dopamine has on the non‐motor symptoms of the disease. PD treatments that focus on the dopaminergic system alone are unable to alleviate both motor and non‐motor symptoms, particularly those that develop at early stages of the disease. The development of agents that interact with several of the affected neurotransmission systems could prove invaluable for the treatment of this disease.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>neurotransmitter</term></item><item><term>non‐motor symptoms</term></item><item><term>Parkinson’s disease</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99/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)1468-1331</doi><issn type="print">1351-5101</issn><issn type="electronic">1468-1331</issn><idGroup><id type="product" value="ENE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROLOGY">European Journal of Neurology</title></titleGroup></publicationMeta><publicationMeta level="part" position="03003"><doi origin="wiley">10.1111/ene.2010.17.issue-3</doi><numberingGroup><numbering type="journalVolume" number="17">17</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="2010-03">March 2010</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="7" status="forIssue"><doi origin="wiley">10.1111/j.1468-1331.2009.02900.x</doi><idGroup><id type="unit" value="ENE2900"></id></idGroup><countGroup><count type="pageTotal" number="13"></count></countGroup><titleGroup><title type="tocHeading1">Review Article</title></titleGroup><copyright>© 2009 The Author(s). Journal compilation © 2009 EFNS</copyright><eventGroup><event type="firstOnline" date="2009-12-30"></event><event type="publishedOnlineFinalForm" date="2010-02-23"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-07"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-24"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-17"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="364">364</numbering><numbering type="pageLast" number="376">376</numbering></numberingGroup><correspondenceTo>Prof. Paolo Barone, Dipartimento di Scienze Neurologiche, Università Federico II, Via Pansini 5, Naples 80131, Italy (tel.: +39 081 7462670; fax: +39 081 546 6596; e‐mail: <email>barone@unina.it</email>).</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ENE.ENE2900.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 29 May 2009 Accepted 3 November 2009</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="2"></count></countGroup><titleGroup><title type="main">Neurotransmission in Parkinson’s disease: beyond dopamine</title><title type="shortAuthors">P. Barone</title><title type="short">Neurotransmission in Parkinson’s disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#aff-1-1"><personName><givenNames>P.</givenNames><familyName>Barone</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="IT"><unparsedAffiliation>Dipartimento di Scienze Neurologiche and IDC‐Hermitage‐Capodimonte, Naples, Italy</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">neurotransmitter</keyword><keyword xml:id="k2">non‐motor symptoms</keyword><keyword xml:id="k3">Parkinson’s disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Parkinson’s disease (PD) is most frequently associated with characteristic motor symptoms that are known to arise with degeneration of dopaminergic neurons. However, patients with this disease also experience a multitude of non‐motor symptoms, such as sleep disturbances, fatigue, apathy, anxiety, depression, cognitive impairment, dementia, olfactory dysfunction, pain, sweating and constipation, some of which can be at least as debilitating as the movement disorders and have a major impact on patients’ quality of life. Many of these non‐motor symptoms may be evident prior to the onset of motor dysfunction. The neuropathology of PD has shown that complex, interconnected neuronal systems, regulated by a number of different neurotransmitters in addition to dopamine, are involved in the aetiology of motor and non‐motor symptoms. This review focuses on the non‐dopaminergic neurotransmission systems associated with PD with particular reference to the effect that their modulation and interaction with dopamine has on the non‐motor symptoms of the disease. PD treatments that focus on the dopaminergic system alone are unable to alleviate both motor and non‐motor symptoms, particularly those that develop at early stages of the disease. The development of agents that interact with several of the affected neurotransmission systems could prove invaluable for the treatment of this disease.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Neurotransmission in Parkinson’s disease: beyond dopamine</title></titleInfo><titleInfo type="abbreviated"><title>Neurotransmission in Parkinson’s disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Neurotransmission in Parkinson’s disease: beyond dopamine</title></titleInfo><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Barone</namePart><affiliation>Dipartimento di Scienze Neurologiche and IDC‐Hermitage‐Capodimonte, Naples, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-03</dateIssued><edition>Received 29 May 2009 Accepted 3 November 2009</edition><copyrightDate encoding="w3cdtf">2010</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></physicalDescription><abstract lang="en">Parkinson’s disease (PD) is most frequently associated with characteristic motor symptoms that are known to arise with degeneration of dopaminergic neurons. However, patients with this disease also experience a multitude of non‐motor symptoms, such as sleep disturbances, fatigue, apathy, anxiety, depression, cognitive impairment, dementia, olfactory dysfunction, pain, sweating and constipation, some of which can be at least as debilitating as the movement disorders and have a major impact on patients’ quality of life. Many of these non‐motor symptoms may be evident prior to the onset of motor dysfunction. The neuropathology of PD has shown that complex, interconnected neuronal systems, regulated by a number of different neurotransmitters in addition to dopamine, are involved in the aetiology of motor and non‐motor symptoms. This review focuses on the non‐dopaminergic neurotransmission systems associated with PD with particular reference to the effect that their modulation and interaction with dopamine has on the non‐motor symptoms of the disease. PD treatments that focus on the dopaminergic system alone are unable to alleviate both motor and non‐motor symptoms, particularly those that develop at early stages of the disease. The development of agents that interact with several of the affected neurotransmission systems could prove invaluable for the treatment of this disease.</abstract><subject lang="en"><genre>Keywords</genre><topic>neurotransmitter</topic><topic>non‐motor symptoms</topic><topic>Parkinson’s disease</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neurology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1351-5101</identifier><identifier type="eISSN">1468-1331</identifier><identifier type="DOI">10.1111/(ISSN)1468-1331</identifier><identifier type="PublisherID">ENE</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>364</start><end>376</end><total>13</total></extent></part></relatedItem><identifier type="istex">DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99</identifier><identifier type="DOI">10.1111/j.1468-1331.2009.02900.x</identifier><identifier type="ArticleID">ENE2900</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2009 The Author(s). Journal compilation © 2009 EFNS</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000278 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000278 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:DEE6F9CE51990424CB5F7E9F64D6C67D497C2B99
|texte= Neurotransmission in Parkinson’s disease: beyond dopamine
}}
| This area was generated with Dilib version V0.6.23. |  |