Molecular imaging and neural networks in impulse control disorders in Parkinson's disease.
Identifieur interne : 000206 ( PubMed/Checkpoint ); précédent : 000205; suivant : 000207Molecular imaging and neural networks in impulse control disorders in Parkinson's disease.
Auteurs : I. Aracil-Bola Os [Canada] ; A P Strafella [Canada]Source :
- Parkinsonism & related disorders [ 1873-5126 ] ; 2016.
English descriptors
- KwdEn :
- Animals, Corpus Striatum (metabolism), Corpus Striatum (pathology), Disruptive, Impulse Control, and Conduct Disorders (chemically induced), Disruptive, Impulse Control, and Conduct Disorders (diagnosis), Disruptive, Impulse Control, and Conduct Disorders (metabolism), Dopamine (metabolism), Dopamine Agonists (adverse effects), Humans, Molecular Imaging (methods), Nerve Net (metabolism), Nerve Net (pathology), Neuroimaging (methods), Parkinson Disease (diagnosis), Parkinson Disease (drug therapy), Parkinson Disease (metabolism).
- MESH :
- chemical , adverse effects : Dopamine Agonists.
- chemical , metabolism : Dopamine.
- chemically induced : Disruptive, Impulse Control, and Conduct Disorders.
- diagnosis : Disruptive, Impulse Control, and Conduct Disorders, Parkinson Disease.
- drug therapy : Parkinson Disease.
- metabolism : Corpus Striatum, Disruptive, Impulse Control, and Conduct Disorders, Nerve Net, Parkinson Disease.
- methods : Molecular Imaging, Neuroimaging.
- pathology : Corpus Striatum, Nerve Net.
- Animals, Humans.
Abstract
Impulse control disorders (ICDs) may arise in Parkinson's disease (PD) in relation to the use of dopamine agonists (DA). A dysfunction of reward circuits is considered the main underlying mechanism. Neuroimaging has been largely used in this setting to understand the structure of the reward system and its abnormalities brought by exogenous stimulation in PD. Dopaminergic changes, such as increased dopamine release, reduced dopamine transporter activity and other changes, have been shown to be a consistent feature of ICDs in PD. Beyond the striatum, alterations of prefrontal cortical function may also impact an individuals' propensity for impulsivity. Neuroimaging is advancing our knowledge of the mechanisms involved in the development of these behavioral addictions. An increased understanding of these disorders may lead to the discovery of new therapeutic targets, or the identification of risk factors for the development of these disorders.
DOI: 10.1016/j.parkreldis.2015.08.003
PubMed: 26298389
Affiliations:
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Aracil-Bola Os</name><affiliation wicri:level="4"><nlm:affiliation>Morton and Gloria Shulman Movement Disorder Unit & Edmond J. Safra Program in Parkinson Disease, Toronto Western Hospital, UHN, University of Toronto, Ontario, Canada; Research Imaging Centre, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada; Division of Brain, Imaging and Behaviour - Systems Neuroscience, Toronto Western Research Institute, UHN, University of Toronto, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Morton and Gloria Shulman Movement Disorder Unit & Edmond J. Safra Program in Parkinson Disease, Toronto Western Hospital, UHN, University of Toronto, Ontario, Canada; Research Imaging Centre, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada; Division of Brain, Imaging and Behaviour - Systems Neuroscience, Toronto Western Research Institute, UHN, University of Toronto, Ontario</wicri:regionArea><orgName type="university">Université de Toronto</orgName><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName></affiliation></author><author><name sortKey="Strafella, A P" sort="Strafella, A P" uniqKey="Strafella A" first="A P" last="Strafella">A P Strafella</name><affiliation wicri:level="4"><nlm:affiliation>Morton and Gloria Shulman Movement Disorder Unit & Edmond J. Safra Program in Parkinson Disease, Toronto Western Hospital, UHN, University of Toronto, Ontario, Canada; Research Imaging Centre, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada; Division of Brain, Imaging and Behaviour - Systems Neuroscience, Toronto Western Research Institute, UHN, University of Toronto, Ontario, Canada. Electronic address: antonio.strafella@uhn.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Morton and Gloria Shulman Movement Disorder Unit & Edmond J. Safra Program in Parkinson Disease, Toronto Western Hospital, UHN, University of Toronto, Ontario, Canada; Research Imaging Centre, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada; Division of Brain, Imaging and Behaviour - Systems Neuroscience, Toronto Western Research Institute, UHN, University of Toronto, Ontario</wicri:regionArea><orgName type="university">Université de Toronto</orgName><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName></affiliation></author></analytic><series><title level="j">Parkinsonism & related disorders</title><idno type="eISSN">1873-5126</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (pathology)</term><term>Disruptive, Impulse Control, and Conduct Disorders (chemically induced)</term><term>Disruptive, Impulse Control, and Conduct Disorders (diagnosis)</term><term>Disruptive, Impulse Control, and Conduct Disorders (metabolism)</term><term>Dopamine (metabolism)</term><term>Dopamine Agonists (adverse effects)</term><term>Humans</term><term>Molecular Imaging (methods)</term><term>Nerve Net (metabolism)</term><term>Nerve Net (pathology)</term><term>Neuroimaging (methods)</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Dopamine Agonists</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Disruptive, Impulse Control, and Conduct Disorders</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Disruptive, Impulse Control, and Conduct Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Disruptive, Impulse Control, and Conduct Disorders</term><term>Nerve Net</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Molecular Imaging</term><term>Neuroimaging</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>Nerve Net</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Impulse control disorders (ICDs) may arise in Parkinson's disease (PD) in relation to the use of dopamine agonists (DA). A dysfunction of reward circuits is considered the main underlying mechanism. Neuroimaging has been largely used in this setting to understand the structure of the reward system and its abnormalities brought by exogenous stimulation in PD. Dopaminergic changes, such as increased dopamine release, reduced dopamine transporter activity and other changes, have been shown to be a consistent feature of ICDs in PD. Beyond the striatum, alterations of prefrontal cortical function may also impact an individuals' propensity for impulsivity. Neuroimaging is advancing our knowledge of the mechanisms involved in the development of these behavioral addictions. An increased understanding of these disorders may lead to the discovery of new therapeutic targets, or the identification of risk factors for the development of these disorders.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26298389</PMID><DateCreated><Year>2015</Year><Month>11</Month><Day>26</Day></DateCreated><DateCompleted><Year>2016</Year><Month>09</Month><Day>12</Day></DateCompleted><DateRevised><Year>2017</Year><Month>01</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-5126</ISSN><JournalIssue CitedMedium="Internet"><Volume>22 Suppl 1</Volume><PubDate><Year>2016</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Parkinsonism & related disorders</Title><ISOAbbreviation>Parkinsonism Relat. Disord.</ISOAbbreviation></Journal><ArticleTitle>Molecular imaging and neural networks in impulse control disorders in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>S101-5</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.parkreldis.2015.08.003</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1353-8020(15)00335-1</ELocationID><Abstract><AbstractText>Impulse control disorders (ICDs) may arise in Parkinson's disease (PD) in relation to the use of dopamine agonists (DA). A dysfunction of reward circuits is considered the main underlying mechanism. Neuroimaging has been largely used in this setting to understand the structure of the reward system and its abnormalities brought by exogenous stimulation in PD. Dopaminergic changes, such as increased dopamine release, reduced dopamine transporter activity and other changes, have been shown to be a consistent feature of ICDs in PD. Beyond the striatum, alterations of prefrontal cortical function may also impact an individuals' propensity for impulsivity. Neuroimaging is advancing our knowledge of the mechanisms involved in the development of these behavioral addictions. An increased understanding of these disorders may lead to the discovery of new therapeutic targets, or the identification of risk factors for the development of these disorders.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aracil-Bolaños</LastName><ForeName>I</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Morton and Gloria Shulman Movement Disorder Unit & Edmond J. Safra Program in Parkinson Disease, Toronto Western Hospital, UHN, University of Toronto, Ontario, Canada; Research Imaging Centre, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada; Division of Brain, Imaging and Behaviour - Systems Neuroscience, Toronto Western Research Institute, UHN, University of Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Strafella</LastName><ForeName>A P</ForeName><Initials>AP</Initials><AffiliationInfo><Affiliation>Morton and Gloria Shulman Movement Disorder Unit & Edmond J. Safra Program in Parkinson Disease, Toronto Western Hospital, UHN, University of Toronto, Ontario, Canada; Research Imaging Centre, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada; Division of Brain, Imaging and Behaviour - Systems Neuroscience, Toronto Western Research Institute, UHN, University of Toronto, Ontario, Canada. Electronic address: antonio.strafella@uhn.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>136778-1</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant><Grant><GrantID>MOP 136778</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>08</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Parkinsonism Relat Disord</MedlineTA><NlmUniqueID>9513583</NlmUniqueID><ISSNLinking>1353-8020</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018491">Dopamine Agonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Brain. 2009 May;132(Pt 5):1366-75</RefSource><PMID Version="1">19153147</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2008 Dec;64 Suppl 2:S93-100</RefSource><PMID Version="1">19127573</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropsychopharmacology. 2009 Dec;34(13):2758-66</RefSource><PMID Version="1">19741594</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Lancet Neurol. 2009 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Aracil-Bola Os</name></region><name sortKey="Strafella, A P" sort="Strafella, A P" uniqKey="Strafella A" first="A P" last="Strafella">A P Strafella</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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