Association between MAPT haplotype and memory function in patients with Parkinson's disease and healthy aging individuals.
Identifieur interne : 000559 ( PubMed/Curation ); précédent : 000558; suivant : 000560Association between MAPT haplotype and memory function in patients with Parkinson's disease and healthy aging individuals.
Auteurs : Sophie E. Winder-Rhodes [Royaume-Uni] ; Adam Hampshire [Royaume-Uni] ; James B. Rowe [Royaume-Uni] ; Jonathan E. Peelle [États-Unis] ; Trevor W. Robbins [Royaume-Uni] ; Adrian M. Owen [Canada] ; Roger A. Barker [Royaume-Uni]Source :
- Neurobiology of aging [ 1558-1497 ] ; 2015.
English descriptors
- KwdEn :
- Aged, Aging (genetics), Aging (psychology), Cognition (physiology), Disease Progression, Female, Genetic Association Studies, Genetic Predisposition to Disease (genetics), Haplotypes (genetics), Humans, Magnetic Resonance Imaging, Male, Memory (physiology), Middle Aged, Oxygen (blood), Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinson Disease (psychology), Risk, Temporal Lobe (pathology), Temporal Lobe (physiopathology), tau Proteins (genetics).
- MESH :
- chemical , blood : Oxygen.
- genetics : Aging, Genetic Predisposition to Disease, Haplotypes, Parkinson Disease, tau Proteins.
- pathology : Parkinson Disease, Temporal Lobe.
- physiology : Cognition, Memory.
- physiopathology : Temporal Lobe.
- psychology : Aging, Parkinson Disease.
- Aged, Disease Progression, Female, Genetic Association Studies, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Risk.
Abstract
Genetic variation is associated with differences in the function of the brain as well as its susceptibility to disease. The common H1 haplotypic variant of the microtubule-associated protein tau gene (MAPT) has been related to an increased risk for Parkinson's disease (PD). Furthermore, among PD patients, H1 homozygotes have an accelerated progression to dementia. We investigated the neurocognitive correlates of MAPT haplotypes using functional magnetic resonance imaging. Thirty-seven nondemented patients with PD (19 H1/H1, 18 H2 carriers) and 40 age-matched controls (21 H1/H1, 19 H2 carriers) were scanned during performance of a picture memory encoding task. Behaviorally, H1 homozygosity was associated with impaired picture recognition memory in PD patients and control subjects. These impairments in the H1 homozygotes were accompanied by an altered blood-oxygen level-dependent response in the medial temporal lobe during successful memory encoding. Additional age-related differences in blood-oxygen level-dependent response were observed in the medial temporal lobes of H1 homozygotes with PD. These results suggest that common variation in MAPT is not only associated with the dementia of PD but also differences in the neural circuitry underlying aspects of cognition in normal aging.
DOI: 10.1016/j.neurobiolaging.2014.12.006
PubMed: 25577413
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Winder-Rhodes</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; Department of Child and Adolescent Psychiatry, Institute of Psychiatry, King's College London, UK. Electronic address: sophie.winder-rhodes@doctors.org.uk.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; Department of Child and Adolescent Psychiatry, Institute of Psychiatry, King's College London</wicri:regionArea></affiliation></author><author><name sortKey="Hampshire, Adam" sort="Hampshire, Adam" uniqKey="Hampshire A" first="Adam" last="Hampshire">Adam Hampshire</name><affiliation wicri:level="1"><nlm:affiliation>MRC Cognition and Brain Sciences Unit, Cambridge, UK; The Division of Brain Sciences, Department of Medicine, Imperial College, London, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Cognition and Brain Sciences Unit, Cambridge, UK; The Division of Brain Sciences, Department of Medicine, Imperial College, London</wicri:regionArea></affiliation></author><author><name sortKey="Rowe, James B" sort="Rowe, James B" uniqKey="Rowe J" first="James B" last="Rowe">James B. Rowe</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; MRC Cognition and Brain Sciences Unit, Cambridge, UK; Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; MRC Cognition and Brain Sciences Unit, Cambridge, UK; Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge</wicri:regionArea></affiliation></author><author><name sortKey="Peelle, Jonathan E" sort="Peelle, Jonathan E" uniqKey="Peelle J" first="Jonathan E" last="Peelle">Jonathan E. 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Owen</name><affiliation wicri:level="1"><nlm:affiliation>MRC Cognition and Brain Sciences Unit, Cambridge, UK; The Brain and Mind Institute, The University of Western Ontario, London Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>MRC Cognition and Brain Sciences Unit, Cambridge, UK; The Brain and Mind Institute, The University of Western Ontario, London Ontario</wicri:regionArea></affiliation></author><author><name sortKey="Barker, Roger A" sort="Barker, Roger A" uniqKey="Barker R" first="Roger A" last="Barker">Roger A. Barker</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK. Electronic address: rab46@cam.ac.uk.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge</wicri:regionArea></affiliation></author></analytic><series><title level="j">Neurobiology of aging</title><idno type="eISSN">1558-1497</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aging (genetics)</term><term>Aging (psychology)</term><term>Cognition (physiology)</term><term>Disease Progression</term><term>Female</term><term>Genetic Association Studies</term><term>Genetic Predisposition to Disease (genetics)</term><term>Haplotypes (genetics)</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Memory (physiology)</term><term>Middle Aged</term><term>Oxygen (blood)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (psychology)</term><term>Risk</term><term>Temporal Lobe (pathology)</term><term>Temporal Lobe (physiopathology)</term><term>tau Proteins (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Oxygen</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Aging</term><term>Genetic Predisposition to Disease</term><term>Haplotypes</term><term>Parkinson Disease</term><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Temporal Lobe</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cognition</term><term>Memory</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Temporal Lobe</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Aging</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Disease Progression</term><term>Female</term><term>Genetic Association Studies</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Risk</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Genetic variation is associated with differences in the function of the brain as well as its susceptibility to disease. The common H1 haplotypic variant of the microtubule-associated protein tau gene (MAPT) has been related to an increased risk for Parkinson's disease (PD). Furthermore, among PD patients, H1 homozygotes have an accelerated progression to dementia. We investigated the neurocognitive correlates of MAPT haplotypes using functional magnetic resonance imaging. Thirty-seven nondemented patients with PD (19 H1/H1, 18 H2 carriers) and 40 age-matched controls (21 H1/H1, 19 H2 carriers) were scanned during performance of a picture memory encoding task. Behaviorally, H1 homozygosity was associated with impaired picture recognition memory in PD patients and control subjects. These impairments in the H1 homozygotes were accompanied by an altered blood-oxygen level-dependent response in the medial temporal lobe during successful memory encoding. Additional age-related differences in blood-oxygen level-dependent response were observed in the medial temporal lobes of H1 homozygotes with PD. These results suggest that common variation in MAPT is not only associated with the dementia of PD but also differences in the neural circuitry underlying aspects of cognition in normal aging.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25577413</PMID><DateCreated><Year>2015</Year><Month>03</Month><Day>02</Day></DateCreated><DateCompleted><Year>2015</Year><Month>11</Month><Day>24</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1558-1497</ISSN><JournalIssue CitedMedium="Internet"><Volume>36</Volume><Issue>3</Issue><PubDate><Year>2015</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Neurobiology of aging</Title><ISOAbbreviation>Neurobiol. Aging</ISOAbbreviation></Journal><ArticleTitle>Association between MAPT haplotype and memory function in patients with Parkinson's disease and healthy aging individuals.</ArticleTitle><Pagination><MedlinePgn>1519-28</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neurobiolaging.2014.12.006</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0197-4580(14)00798-2</ELocationID><Abstract><AbstractText>Genetic variation is associated with differences in the function of the brain as well as its susceptibility to disease. The common H1 haplotypic variant of the microtubule-associated protein tau gene (MAPT) has been related to an increased risk for Parkinson's disease (PD). Furthermore, among PD patients, H1 homozygotes have an accelerated progression to dementia. We investigated the neurocognitive correlates of MAPT haplotypes using functional magnetic resonance imaging. Thirty-seven nondemented patients with PD (19 H1/H1, 18 H2 carriers) and 40 age-matched controls (21 H1/H1, 19 H2 carriers) were scanned during performance of a picture memory encoding task. Behaviorally, H1 homozygosity was associated with impaired picture recognition memory in PD patients and control subjects. These impairments in the H1 homozygotes were accompanied by an altered blood-oxygen level-dependent response in the medial temporal lobe during successful memory encoding. Additional age-related differences in blood-oxygen level-dependent response were observed in the medial temporal lobes of H1 homozygotes with PD. These results suggest that common variation in MAPT is not only associated with the dementia of PD but also differences in the neural circuitry underlying aspects of cognition in normal aging.</AbstractText><CopyrightInformation>Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Winder-Rhodes</LastName><ForeName>Sophie E</ForeName><Initials>SE</Initials><AffiliationInfo><Affiliation>Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; Department of Child and Adolescent Psychiatry, Institute of Psychiatry, King's College London, UK. Electronic address: sophie.winder-rhodes@doctors.org.uk.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hampshire</LastName><ForeName>Adam</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>MRC Cognition and Brain Sciences Unit, Cambridge, UK; The Division of Brain Sciences, Department of Medicine, Imperial College, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rowe</LastName><ForeName>James B</ForeName><Initials>JB</Initials><AffiliationInfo><Affiliation>Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; MRC Cognition and Brain Sciences Unit, Cambridge, UK; Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peelle</LastName><ForeName>Jonathan E</ForeName><Initials>JE</Initials><AffiliationInfo><Affiliation>Department of Otolaryngology, Washington University in St. Louis, St. Louis, MO, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Robbins</LastName><ForeName>Trevor W</ForeName><Initials>TW</Initials><AffiliationInfo><Affiliation>Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Owen</LastName><ForeName>Adrian M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>MRC Cognition and Brain Sciences Unit, Cambridge, UK; The Brain and Mind Institute, The University of Western Ontario, London Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barker</LastName><ForeName>Roger A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK; Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK. Electronic address: rab46@cam.ac.uk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>G0001354</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>MC_U105597119</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>Department of Health</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>088324</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>103838</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>12</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Aging</MedlineTA><NlmUniqueID>8100437</NlmUniqueID><ISSNLinking>0197-4580</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C054369">MAPT protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>S88TT14065</RegistryNumber><NameOfSubstance UI="D010100">Oxygen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Neuroimage. 2011 Feb 1;54(3):2446-61</RefSource><PMID Version="1">20869446</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Alzheimers Dis. 2010;22(4):1065-71</RefSource><PMID 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MajorTopicYN="N">Risk</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013702" MajorTopicYN="N">Temporal Lobe</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016875" MajorTopicYN="N">tau Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4353560</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Aging</Keyword><Keyword MajorTopicYN="N">Cognitive impairment</Keyword><Keyword MajorTopicYN="N">Dementia</Keyword><Keyword MajorTopicYN="N">Genetics</Keyword><Keyword MajorTopicYN="N">Hippocampus</Keyword><Keyword MajorTopicYN="N">MAPT</Keyword><Keyword MajorTopicYN="N">Memory</Keyword><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">Picture recognition</Keyword><Keyword MajorTopicYN="N">Tau</Keyword><Keyword MajorTopicYN="N">fMRI</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>03</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>11</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>12</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>1</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>1</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25577413</ArticleId><ArticleId IdType="pii">S0197-4580(14)00798-2</ArticleId><ArticleId IdType="doi">10.1016/j.neurobiolaging.2014.12.006</ArticleId><ArticleId IdType="pmc">PMC4353560</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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