Combined insular and striatal dopamine dysfunction are associated with executive deficits in Parkinson's disease with mild cognitive impairment.
Identifieur interne : 000792 ( PubMed/Corpus ); précédent : 000791; suivant : 000793Combined insular and striatal dopamine dysfunction are associated with executive deficits in Parkinson's disease with mild cognitive impairment.
Auteurs : Leigh Christopher ; Connie Marras ; Sarah Duff-Canning ; Yuko Koshimori ; Robert Chen ; Isabelle Boileau ; Barbara Segura ; Oury Monchi ; Anthony E. Lang ; Pablo Rusjan ; Sylvain Houle ; Antonio P. StrafellaSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2014.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Cerebral Cortex (diagnostic imaging), Cerebral Cortex (metabolism), Cerebral Cortex (physiopathology), Cognitive Dysfunction (metabolism), Cognitive Dysfunction (physiopathology), Cognitive Dysfunction (psychology), Corpus Striatum (diagnostic imaging), Corpus Striatum (metabolism), Corpus Striatum (physiopathology), Dopamine D2 Receptor Antagonists, Executive Function (physiology), Female, Humans, Male, Middle Aged, Neuropsychological Tests, Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Parkinson Disease (psychology), Positron-Emission Tomography (methods), Receptors, Dopamine D2 (genetics), Receptors, Dopamine D2 (metabolism).
- MESH :
- chemical , genetics : Receptors, Dopamine D2.
- chemical , metabolism : Receptors, Dopamine D2.
- chemical : Dopamine D2 Receptor Antagonists.
- diagnostic imaging : Cerebral Cortex, Corpus Striatum.
- metabolism : Cerebral Cortex, Cognitive Dysfunction, Corpus Striatum, Parkinson Disease.
- methods : Positron-Emission Tomography.
- physiology : Executive Function.
- physiopathology : Cerebral Cortex, Cognitive Dysfunction, Corpus Striatum, Parkinson Disease.
- psychology : Cognitive Dysfunction, Parkinson Disease.
- Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Neuropsychological Tests.
Abstract
The ability to dynamically use various aspects of cognition is essential to daily function, and reliant on dopaminergic transmission in cortico-striatal circuitry. Our aim was to investigate both striatal and cortical dopaminergic changes in patients with Parkinson's disease with mild cognitive impairment, who represent a vulnerable group for the development of dementia. We hypothesized severe striatal dopamine denervation in the associative (i.e. cognitive) region and cortical D2 receptor abnormalities in the salience and executive networks in Parkinson's disease with mild cognitive impairment compared with cognitively normal patients with Parkinson's disease and healthy control subjects. We used positron emission tomography imaging with dopaminergic ligands (11)C-dihydrotetrabenazine, to investigate striatal dopamine neuron integrity in the associative subdivision and (11)C-FLB 457, to investigate cortical D2 receptor availability in patients with Parkinson's disease (55-80 years of age) with mild cognitive impairment (n = 11), cognitively normal patients with Parkinson's disease (n = 11) and age-matched healthy control subjects (n = 14). Subjects were administered a neuropsychological test battery to assess cognitive status and determine the relationship between dopaminergic changes and cognitive performance. We found that patients with mild cognitive impairment had severe striatal dopamine depletion in the associative (i.e. cognitive) subdivision as well as reduced D2 receptor availability in the bilateral insula, a key cognitive hub, compared to cognitively normal patients and healthy subjects after controlling for age, disease severity and daily dopaminergic medication intake. Associative striatal dopamine depletion was predictive of D2 receptor loss in the insula of patients with Parkinson's disease with mild cognitive impairment, demonstrating interrelated striatal and cortical changes. Insular D2 levels also predicted executive abilities in these patients as measured using a composite executive z-score obtained from neuropsychological testing. Furthermore we assessed cortical thickness to ensure that D2 receptor changes were not confounded by brain atrophy. There was no difference between groups in cortical thickness in the insula, or any other cortical region of interest. These findings suggest that striatal dopamine denervation combined with insular D2 receptor loss underlie mild cognitive impairment in Parkinson's disease and in particular decline in executive function. Furthermore, these findings suggest a crucial and direct role for dopaminergic modulation in the insula in facilitating cognitive function.
DOI: 10.1093/brain/awt337
PubMed: 24334314
Links to Exploration step
pubmed:24334314Le document en format XML
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Safra Parkinson Disease Program, Toronto Western Hospital, UHN, University of Toronto, Ontario, M5T 2S8, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Marras, Connie" sort="Marras, Connie" uniqKey="Marras C" first="Connie" last="Marras">Connie Marras</name></author><author><name sortKey="Duff Canning, Sarah" sort="Duff Canning, Sarah" uniqKey="Duff Canning S" first="Sarah" last="Duff-Canning">Sarah Duff-Canning</name></author><author><name sortKey="Koshimori, Yuko" sort="Koshimori, Yuko" uniqKey="Koshimori Y" first="Yuko" last="Koshimori">Yuko Koshimori</name></author><author><name sortKey="Chen, Robert" sort="Chen, Robert" uniqKey="Chen R" first="Robert" last="Chen">Robert Chen</name></author><author><name sortKey="Boileau, Isabelle" sort="Boileau, Isabelle" uniqKey="Boileau I" first="Isabelle" last="Boileau">Isabelle Boileau</name></author><author><name sortKey="Segura, Barbara" sort="Segura, Barbara" uniqKey="Segura B" first="Barbara" last="Segura">Barbara Segura</name></author><author><name sortKey="Monchi, Oury" sort="Monchi, Oury" uniqKey="Monchi O" first="Oury" last="Monchi">Oury Monchi</name></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. 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Safra Parkinson Disease Program, Toronto Western Hospital, UHN, University of Toronto, Ontario, M5T 2S8, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Marras, Connie" sort="Marras, Connie" uniqKey="Marras C" first="Connie" last="Marras">Connie Marras</name></author><author><name sortKey="Duff Canning, Sarah" sort="Duff Canning, Sarah" uniqKey="Duff Canning S" first="Sarah" last="Duff-Canning">Sarah Duff-Canning</name></author><author><name sortKey="Koshimori, Yuko" sort="Koshimori, Yuko" uniqKey="Koshimori Y" first="Yuko" last="Koshimori">Yuko Koshimori</name></author><author><name sortKey="Chen, Robert" sort="Chen, Robert" uniqKey="Chen R" first="Robert" last="Chen">Robert Chen</name></author><author><name sortKey="Boileau, Isabelle" sort="Boileau, Isabelle" uniqKey="Boileau I" first="Isabelle" last="Boileau">Isabelle Boileau</name></author><author><name sortKey="Segura, Barbara" sort="Segura, Barbara" uniqKey="Segura B" first="Barbara" last="Segura">Barbara Segura</name></author><author><name sortKey="Monchi, Oury" sort="Monchi, Oury" uniqKey="Monchi O" first="Oury" last="Monchi">Oury Monchi</name></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. Lang</name></author><author><name sortKey="Rusjan, Pablo" sort="Rusjan, Pablo" uniqKey="Rusjan P" first="Pablo" last="Rusjan">Pablo Rusjan</name></author><author><name sortKey="Houle, Sylvain" sort="Houle, Sylvain" uniqKey="Houle S" first="Sylvain" last="Houle">Sylvain Houle</name></author><author><name sortKey="Strafella, Antonio P" sort="Strafella, Antonio P" uniqKey="Strafella A" first="Antonio P" last="Strafella">Antonio P. Strafella</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Cerebral Cortex (diagnostic imaging)</term><term>Cerebral Cortex (metabolism)</term><term>Cerebral Cortex (physiopathology)</term><term>Cognitive Dysfunction (metabolism)</term><term>Cognitive Dysfunction (physiopathology)</term><term>Cognitive Dysfunction (psychology)</term><term>Corpus Striatum (diagnostic imaging)</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (physiopathology)</term><term>Dopamine D2 Receptor Antagonists</term><term>Executive Function (physiology)</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (psychology)</term><term>Positron-Emission Tomography (methods)</term><term>Receptors, Dopamine D2 (genetics)</term><term>Receptors, Dopamine D2 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Dopamine D2 Receptor Antagonists</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Cerebral Cortex</term><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cerebral Cortex</term><term>Cognitive Dysfunction</term><term>Corpus Striatum</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Positron-Emission Tomography</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Executive Function</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebral Cortex</term><term>Cognitive Dysfunction</term><term>Corpus Striatum</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Cognitive Dysfunction</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The ability to dynamically use various aspects of cognition is essential to daily function, and reliant on dopaminergic transmission in cortico-striatal circuitry. Our aim was to investigate both striatal and cortical dopaminergic changes in patients with Parkinson's disease with mild cognitive impairment, who represent a vulnerable group for the development of dementia. We hypothesized severe striatal dopamine denervation in the associative (i.e. cognitive) region and cortical D2 receptor abnormalities in the salience and executive networks in Parkinson's disease with mild cognitive impairment compared with cognitively normal patients with Parkinson's disease and healthy control subjects. We used positron emission tomography imaging with dopaminergic ligands (11)C-dihydrotetrabenazine, to investigate striatal dopamine neuron integrity in the associative subdivision and (11)C-FLB 457, to investigate cortical D2 receptor availability in patients with Parkinson's disease (55-80 years of age) with mild cognitive impairment (n = 11), cognitively normal patients with Parkinson's disease (n = 11) and age-matched healthy control subjects (n = 14). Subjects were administered a neuropsychological test battery to assess cognitive status and determine the relationship between dopaminergic changes and cognitive performance. We found that patients with mild cognitive impairment had severe striatal dopamine depletion in the associative (i.e. cognitive) subdivision as well as reduced D2 receptor availability in the bilateral insula, a key cognitive hub, compared to cognitively normal patients and healthy subjects after controlling for age, disease severity and daily dopaminergic medication intake. Associative striatal dopamine depletion was predictive of D2 receptor loss in the insula of patients with Parkinson's disease with mild cognitive impairment, demonstrating interrelated striatal and cortical changes. Insular D2 levels also predicted executive abilities in these patients as measured using a composite executive z-score obtained from neuropsychological testing. Furthermore we assessed cortical thickness to ensure that D2 receptor changes were not confounded by brain atrophy. There was no difference between groups in cortical thickness in the insula, or any other cortical region of interest. These findings suggest that striatal dopamine denervation combined with insular D2 receptor loss underlie mild cognitive impairment in Parkinson's disease and in particular decline in executive function. Furthermore, these findings suggest a crucial and direct role for dopaminergic modulation in the insula in facilitating cognitive function.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24334314</PMID><DateCreated><Year>2014</Year><Month>02</Month><Day>06</Day></DateCreated><DateCompleted><Year>2014</Year><Month>04</Month><Day>11</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2156</ISSN><JournalIssue CitedMedium="Internet"><Volume>137</Volume><Issue>Pt 2</Issue><PubDate><Year>2014</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Combined insular and striatal dopamine dysfunction are associated with executive deficits in Parkinson's disease with mild cognitive impairment.</ArticleTitle><Pagination><MedlinePgn>565-75</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/brain/awt337</ELocationID><Abstract><AbstractText>The ability to dynamically use various aspects of cognition is essential to daily function, and reliant on dopaminergic transmission in cortico-striatal circuitry. Our aim was to investigate both striatal and cortical dopaminergic changes in patients with Parkinson's disease with mild cognitive impairment, who represent a vulnerable group for the development of dementia. We hypothesized severe striatal dopamine denervation in the associative (i.e. cognitive) region and cortical D2 receptor abnormalities in the salience and executive networks in Parkinson's disease with mild cognitive impairment compared with cognitively normal patients with Parkinson's disease and healthy control subjects. We used positron emission tomography imaging with dopaminergic ligands (11)C-dihydrotetrabenazine, to investigate striatal dopamine neuron integrity in the associative subdivision and (11)C-FLB 457, to investigate cortical D2 receptor availability in patients with Parkinson's disease (55-80 years of age) with mild cognitive impairment (n = 11), cognitively normal patients with Parkinson's disease (n = 11) and age-matched healthy control subjects (n = 14). Subjects were administered a neuropsychological test battery to assess cognitive status and determine the relationship between dopaminergic changes and cognitive performance. We found that patients with mild cognitive impairment had severe striatal dopamine depletion in the associative (i.e. cognitive) subdivision as well as reduced D2 receptor availability in the bilateral insula, a key cognitive hub, compared to cognitively normal patients and healthy subjects after controlling for age, disease severity and daily dopaminergic medication intake. Associative striatal dopamine depletion was predictive of D2 receptor loss in the insula of patients with Parkinson's disease with mild cognitive impairment, demonstrating interrelated striatal and cortical changes. Insular D2 levels also predicted executive abilities in these patients as measured using a composite executive z-score obtained from neuropsychological testing. Furthermore we assessed cortical thickness to ensure that D2 receptor changes were not confounded by brain atrophy. There was no difference between groups in cortical thickness in the insula, or any other cortical region of interest. These findings suggest that striatal dopamine denervation combined with insular D2 receptor loss underlie mild cognitive impairment in Parkinson's disease and in particular decline in executive function. Furthermore, these findings suggest a crucial and direct role for dopaminergic modulation in the insula in facilitating cognitive function.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Christopher</LastName><ForeName>Leigh</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>1 Morton and Gloria Shulman Movement Disorder Unit and E.J. Safra Parkinson Disease Program, Toronto Western Hospital, UHN, University of Toronto, Ontario, M5T 2S8, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Marras</LastName><ForeName>Connie</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Duff-Canning</LastName><ForeName>Sarah</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Koshimori</LastName><ForeName>Yuko</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Robert</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Boileau</LastName><ForeName>Isabelle</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Segura</LastName><ForeName>Barbara</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Monchi</LastName><ForeName>Oury</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Lang</LastName><ForeName>Anthony E</ForeName><Initials>AE</Initials></Author><Author ValidYN="Y"><LastName>Rusjan</LastName><ForeName>Pablo</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Houle</LastName><ForeName>Sylvain</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Strafella</LastName><ForeName>Antonio P</ForeName><Initials>AP</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>110962-1</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant><Grant><GrantID>MOP 110962</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></PublicationTypeList><ArticleDate 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Version="1">8331222</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurosci Biobehav Rev. 2006;30(1):1-23</RefSource><PMID Version="1">15935475</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Struct Funct. 2010 Jun;214(5-6):655-67</RefSource><PMID Version="1">20512370</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Prog Neurobiol. 2004 Sep;74(1):1-58</RefSource><PMID Version="1">15381316</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Nucl Med. 1999 Feb;40(2):283-9</RefSource><PMID Version="1">10025836</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002540" MajorTopicYN="N">Cerebral 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