Association between MAPT haplotype and memory function in patients with Parkinson's disease and healthy aging individuals
Identifieur interne : 000355 ( Pmc/Checkpoint ); précédent : 000354; suivant : 000356Association 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 [Royaume-Uni, Canada] ; Roger A. Barker [Royaume-Uni]Source :
- Neurobiology of Aging [ 0197-4580 ] ; 2015.
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 (
Url:
DOI: 10.1016/j.neurobiolaging.2014.12.006
PubMed: 25577413
PubMed Central: 4353560
Affiliations:
- Canada, Royaume-Uni, États-Unis
- Angleterre, Angleterre de l'Est, Grand Londres, Missouri (État)
- Cambridge, Londres, Saint-Louis (Missouri)
- Université Washington de Saint-Louis, Université de Cambridge
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Winder-Rhodes</name><affiliation wicri:level="4"><nlm:aff id="aff1">Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neurosciences, University of Cambridge, Cambridge</wicri:regionArea><orgName type="university">Université de Cambridge</orgName><placeName><settlement type="city">Cambridge</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Angleterre de l'Est</region></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2">Department of Child and Adolescent Psychiatry, Institute of Psychiatry, King's College London, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Child and Adolescent Psychiatry, Institute of Psychiatry, King's College London</wicri:regionArea><wicri:noRegion>King's College London</wicri:noRegion></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:aff id="aff3">MRC Cognition and Brain Sciences Unit, Cambridge, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Cognition and Brain Sciences Unit, Cambridge</wicri:regionArea><wicri:noRegion>Cambridge</wicri:noRegion></affiliation><affiliation wicri:level="3"><nlm:aff id="aff4">The Division of Brain Sciences, Department of Medicine, Imperial College, London, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>The Division of Brain Sciences, Department of Medicine, Imperial College, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></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="4"><nlm:aff id="aff1">Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neurosciences, University of Cambridge, Cambridge</wicri:regionArea><orgName type="university">Université de Cambridge</orgName><placeName><settlement type="city">Cambridge</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Angleterre de l'Est</region></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3">MRC Cognition and Brain Sciences Unit, Cambridge, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Cognition and Brain Sciences Unit, Cambridge</wicri:regionArea><wicri:noRegion>Cambridge</wicri:noRegion></affiliation><affiliation wicri:level="4"><nlm:aff id="aff5">Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge</wicri:regionArea><orgName type="university">Université de Cambridge</orgName><placeName><settlement type="city">Cambridge</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Angleterre de l'Est</region></placeName></affiliation></author><author><name sortKey="Peelle, Jonathan E" sort="Peelle, Jonathan E" uniqKey="Peelle J" first="Jonathan E." last="Peelle">Jonathan E. Peelle</name><affiliation wicri:level="4"><nlm:aff id="aff6">Department of Otolaryngology, Washington University in St. Louis, St. Louis, MO, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Otolaryngology, Washington University in St. Louis, St. Louis, MO</wicri:regionArea><orgName type="university">Université Washington de Saint-Louis</orgName><placeName><settlement type="city">Saint-Louis (Missouri)</settlement><region type="state">Missouri (État)</region></placeName></affiliation></author><author><name sortKey="Robbins, Trevor W" sort="Robbins, Trevor W" uniqKey="Robbins T" first="Trevor W." last="Robbins">Trevor W. Robbins</name><affiliation wicri:level="4"><nlm:aff id="aff5">Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge</wicri:regionArea><orgName type="university">Université de Cambridge</orgName><placeName><settlement type="city">Cambridge</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Angleterre de l'Est</region></placeName></affiliation></author><author><name sortKey="Owen, Adrian M" sort="Owen, Adrian M" uniqKey="Owen A" first="Adrian M." last="Owen">Adrian M. Owen</name><affiliation wicri:level="1"><nlm:aff id="aff3">MRC Cognition and Brain Sciences Unit, Cambridge, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Cognition and Brain Sciences Unit, Cambridge</wicri:regionArea><wicri:noRegion>Cambridge</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff7">The Brain and Mind Institute, The University of Western Ontario, London Ontario, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>The Brain and Mind Institute, The University of Western Ontario, London Ontario</wicri:regionArea><wicri:noRegion>London Ontario</wicri:noRegion></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="4"><nlm:aff id="aff1">Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neurosciences, University of Cambridge, Cambridge</wicri:regionArea><orgName type="university">Université de Cambridge</orgName><placeName><settlement type="city">Cambridge</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Angleterre de l'Est</region></placeName></affiliation><affiliation wicri:level="4"><nlm:aff id="aff5">Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK</nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge</wicri:regionArea><orgName type="university">Université de Cambridge</orgName><placeName><settlement type="city">Cambridge</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Angleterre de l'Est</region></placeName></affiliation></author></analytic><series><title level="j">Neurobiology of Aging</title><idno type="ISSN">0197-4580</idno><idno type="eISSN">1558-1497</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>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 (<italic>MAPT</italic>) 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 <italic>MAPT</italic> 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 <italic>MAPT</italic> is not only associated with the dementia of PD but also differences in the neural circuitry underlying aspects of cognition in normal aging.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Aarsland, D" uniqKey="Aarsland D">D. Aarsland</name></author><author><name sortKey="Andersen, K" uniqKey="Andersen K">K. Andersen</name></author><author><name sortKey="Larsen, J P" uniqKey="Larsen J">J.P. Larsen</name></author><author><name sortKey="Lolk, A" uniqKey="Lolk A">A. Lolk</name></author><author><name sortKey="Kragh S Rensen, P" uniqKey="Kragh S Rensen P">P. Kragh-Sørensen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Aarsland, D" uniqKey="Aarsland D">D. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Neurobiol Aging</journal-id><journal-id journal-id-type="iso-abbrev">Neurobiol. Aging</journal-id><journal-title-group><journal-title>Neurobiology of Aging</journal-title></journal-title-group><issn pub-type="ppub">0197-4580</issn><issn pub-type="epub">1558-1497</issn><publisher><publisher-name>Elsevier</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">25577413</article-id><article-id pub-id-type="pmc">4353560</article-id><article-id pub-id-type="publisher-id">S0197-4580(14)00798-2</article-id><article-id pub-id-type="doi">10.1016/j.neurobiolaging.2014.12.006</article-id><article-categories><subj-group subj-group-type="heading"><subject>Regular Article</subject></subj-group></article-categories><title-group><article-title>Association between <italic>MAPT</italic> haplotype and memory function in patients with Parkinson's disease and healthy aging individuals</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Winder-Rhodes</surname><given-names>Sophie E.</given-names></name><email>sophie.winder-rhodes@doctors.org.uk</email><xref rid="aff1" ref-type="aff">a</xref><xref rid="aff2" ref-type="aff">b</xref><xref rid="cor1" ref-type="corresp">∗</xref></contrib><contrib contrib-type="author"><name><surname>Hampshire</surname><given-names>Adam</given-names></name><xref rid="aff3" ref-type="aff">c</xref><xref rid="aff4" ref-type="aff">d</xref></contrib><contrib contrib-type="author"><name><surname>Rowe</surname><given-names>James B.</given-names></name><xref rid="aff1" ref-type="aff">a</xref><xref rid="aff3" ref-type="aff">c</xref><xref rid="aff5" ref-type="aff">e</xref></contrib><contrib contrib-type="author"><name><surname>Peelle</surname><given-names>Jonathan E.</given-names></name><xref rid="aff6" ref-type="aff">f</xref></contrib><contrib contrib-type="author"><name><surname>Robbins</surname><given-names>Trevor W.</given-names></name><xref rid="aff5" ref-type="aff">e</xref></contrib><contrib contrib-type="author"><name><surname>Owen</surname><given-names>Adrian M.</given-names></name><xref rid="aff3" ref-type="aff">c</xref><xref rid="aff7" ref-type="aff">g</xref></contrib><contrib contrib-type="author"><name><surname>Barker</surname><given-names>Roger A.</given-names></name><email>rab46@cam.ac.uk</email><xref rid="aff1" ref-type="aff">a</xref><xref rid="aff5" ref-type="aff">e</xref><xref rid="cor2" ref-type="corresp">∗∗</xref></contrib></contrib-group><aff id="aff1"><label>a</label>Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK</aff><aff id="aff2"><label>b</label>Department of Child and Adolescent Psychiatry, Institute of Psychiatry, King's College London, UK</aff><aff id="aff3"><label>c</label>MRC Cognition and Brain Sciences Unit, Cambridge, UK</aff><aff id="aff4"><label>d</label>The Division of Brain Sciences, Department of Medicine, Imperial College, London, UK</aff><aff id="aff5"><label>e</label>Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK</aff><aff id="aff6"><label>f</label>Department of Otolaryngology, Washington University in St. Louis, St. Louis, MO, USA</aff><aff id="aff7"><label>g</label>The Brain and Mind Institute, The University of Western Ontario, London Ontario, Canada</aff><author-notes><corresp id="cor1"><label>∗</label>Corresponding author at: Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0PY, UK. <email>sophie.winder-rhodes@doctors.org.uk</email></corresp><corresp id="cor2"><label>∗∗</label>Alternate corresponding author at: Department of Clinical Neurosciences, University of Cambridge, Cambridge, CB2 0PY, UK. Tel.: +44 1223 331160; fax: +44 1223 331174. <email>rab46@cam.ac.uk</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>1</day><month>3</month><year>2015</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>3</month><year>2015</year></pub-date><volume>36</volume><issue>3</issue><fpage>1519</fpage><lpage>1528</lpage><history><date date-type="received"><day>27</day><month>3</month><year>2014</year></date><date date-type="rev-recd"><day>27</day><month>11</month><year>2014</year></date><date date-type="accepted"><day>4</day><month>12</month><year>2014</year></date></history><permissions><copyright-statement>© 2015 The Authors</copyright-statement><copyright-year>2015</copyright-year><license license-type="CC BY" xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).</license-p></license></permissions><abstract><p>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 (<italic>MAPT</italic>) 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 <italic>MAPT</italic> 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 <italic>MAPT</italic> is not only associated with the dementia of PD but also differences in the neural circuitry underlying aspects of cognition in normal aging.</p></abstract><kwd-group><title>Keywords</title><kwd>Parkinson's disease</kwd><kwd>Dementia</kwd><kwd>Aging</kwd><kwd>Memory</kwd><kwd>fMRI</kwd><kwd>Hippocampus</kwd><kwd><italic>MAPT</italic></kwd><kwd>Genetics</kwd><kwd>Tau</kwd><kwd>Cognitive impairment</kwd><kwd>Picture recognition</kwd></kwd-group></article-meta></front><floats-group><fig id="fig1"><label>Fig. 1</label><caption><p>The abstract pictures memory encoding task. (A) A typical series of stimuli. (B) A typical presentation in the post-scanner test of recognition. Participants responded using the arrow keys on the keyboard. (C) Performance on the post-scanner test of recognition. d’ scores are shown (higher score represents greater discrimination during recognition memory). Group means are plotted. Error bars indicate ± 1 SEM. Asterisk denotes <italic>p</italic> < 0.05 based on main effects of repeated measures ANOVAs. There were additional significant effects of the number of presentations and disease status (PD patients vs. control subjects). Abbreviations: ANOVA, analysis of variance; PD, Parkinson's disease; SEM, standard error of the mean.</p></caption><graphic xlink:href="gr1"></graphic></fig><fig id="fig2"><label>Fig. 2</label><caption><p>Activation in the hippocampal regions of interest (ROI) during successful encoding (contrast 1: successful minus unsuccessful encoding) in all participants stratified by <italic>MAPT</italic> haplotype. ROIs were defined anatomically using AAL templates, and activation is expressed in arbitrary units using the mean parameter estimates from the ROI. *<italic>p</italic> < 0.05 (2-tailed <italic>t</italic> tests). Error bars indicate ± 1 SEM. Abbreviations: AAL, anatomical labeling atlas; PD, Parkinson's disease; SEM, standard error of the mean.</p></caption><graphic xlink:href="gr2"></graphic></fig><fig id="fig3"><label>Fig. 3</label><caption><p>BOLD activations associated with performance of the memory encoding task. (A) Contrast 1: Activation during successful encoding (i.e. remembered minus non-remembered pictures) across all participants. (B) Effect of <italic>MAPT</italic> haplotype on Contrast 1 activation in patients with PD. (C) Effect of <italic>MAPT</italic> haplotype on Contrast 1 activation in control subjects. (D) Interaction between <italic>MAPT</italic> haplotype and PD (PD patients vs. control subjects) on Contrast 1 activation. (E) Contrast 2: Activation during overall task performance minus rest across all participants. (F) Effect of <italic>MAPT</italic> haplotype on Contrast 2 activation in patients with PD. (G) Effect of <italic>MAPT</italic> haplotype on Contrast 2 activation in control subjects. (H) Interaction between <italic>MAPT</italic> haplotype and PD (PD patients vs. control subjects) on Contrast 2 activation. All effects of <italic>MAPT</italic> correspond with increased activation in H2 carriers compared with H1 homozygotes (H1/H1). Activation that survived permutation-based cluster correction (<italic>p</italic> < 0.05 FWE corrected) within a predefined inclusive mask of the temporal lobe region of interest (green) is displayed. Abbreviations: BOLD, blood-oxygen level-dependent; PD, Parkinson's disease.</p></caption><graphic xlink:href="gr3"></graphic></fig><fig id="fig4"><label>Fig. 4</label><caption><p>Correlations between age and hippocampal activation during overall task performance. Mean activation data for contrast 2 (“all events minus baseline”) was extracted from peak activation coordinates defined in contrast 1 (“successful encoding”). Values are plotted after winsorizing one outlier (>2.5 SD from mean) in the group of H1 homozygotes (H1/H1) with Parkinson's disease (PD). A significant negative correlation (<italic>p</italic> < 0.05) between age and activation is seen in H1 homozygotes with PD. Abbreviation: SD, standard deviation.</p></caption><graphic xlink:href="gr4"></graphic></fig><table-wrap id="tbl1" position="float"><label>Table 1</label><caption><p>Clinical and demographic characteristics of the participants</p></caption><table frame="hsides" rules="groups"><thead><tr><th rowspan="2">Variable</th><th colspan="2">Controls<hr></hr></th><th colspan="2">PD patients<hr></hr></th><th colspan="3"><italic>p</italic>-value of group differences<hr></hr></th></tr><tr><th>H1/H1</th><th>H2 carriers</th><th>H1/H1</th><th>H2 carriers</th><th>All groups</th><th><italic>MAPT</italic></th><th>PD vs. control</th></tr></thead><tbody><tr><td>N</td><td>21</td><td>19</td><td>19</td><td>18</td><td>—</td><td>—</td><td>—</td></tr><tr><td>Sex (male: female)</td><td>13:8</td><td>11:8</td><td>11:8</td><td>12:6</td><td align="char">0.94</td><td align="char">0.85</td><td align="char">0.85</td></tr><tr><td>Age (y)</td><td>62.6 ± 5.6</td><td>65.7 ± 4.8</td><td>64.0 ± 7.2</td><td>63.6 ± 7.0</td><td align="char">0.45</td><td align="char">0.31</td><td align="char">0.81</td></tr><tr><td>ACE-R (%)</td><td>92.6 ± 2.4</td><td>95.8 ± 3.0</td><td>95.4 ± 3.8</td><td>94.9 ± 3.5</td><td align="char">0.14</td><td align="char">0.98</td><td align="char">0.07</td></tr><tr><td>ACE-R memory (/26)</td><td>24.5 ± 1.9</td><td>24.0 ± 2.4</td><td>24.2 ± 1.9</td><td>23.7 ± 2.9</td><td align="char">0.76</td><td align="char">0.37</td><td align="char">0.55</td></tr><tr><td>BDI</td><td>4.2 ± 4.3</td><td>5.5 ± 5.0</td><td>6.2 ± 3.0</td><td>8.7 ± 5.3</td><td align="char">0.03</td><td align="char">0.09</td><td align="char">0.02</td></tr><tr><td>NART</td><td>122.4 ± 4.7</td><td>121.9 ± 6.4</td><td>117.9 ± 8.0</td><td>117.2 ± 8.3</td><td align="char">0.05</td><td align="char">0.69</td><td align="char">0.01</td></tr><tr><td>Years of education</td><td>15.3 ± 3.5</td><td>15.1 ± 3.0</td><td>13.7 ± 2.9</td><td>13.9 ± 3.4</td><td align="char">0.38</td><td align="char">0.96</td><td align="char">0.08</td></tr><tr><td>H&Y</td><td>NA</td><td>NA</td><td>1.8 ± 0.4</td><td>1.7 ± 0.5</td><td align="char">0.65</td><td align="char">0.65</td><td>NA</td></tr><tr><td>MDS-UPDRS 3</td><td>NA</td><td>NA</td><td>28.2 ± 11.0</td><td>28.0 ± 12.4</td><td align="char">0.97</td><td align="char">0.97</td><td>NA</td></tr><tr><td>Years since diagnosis</td><td>NA</td><td>NA</td><td>6.7 ± 2.4</td><td>6.8 ± 4.0</td><td align="char">0.98</td><td align="char">0.98</td><td>NA</td></tr><tr><td>Actual L-dopa (mg)</td><td>NA</td><td>NA</td><td>329.0 ± 231.7</td><td>361.9 ± 208.2</td><td align="char">0.65</td><td align="char">0.65</td><td>NA</td></tr><tr><td>Equivalent L-dopa (mg)</td><td>NA</td><td>NA</td><td>1202.6 ± 685.2</td><td>939.7 ± 526.4</td><td align="char">0.20</td><td align="char">0.20</td><td>NA</td></tr></tbody></table><table-wrap-foot><fn><p>Values are expressed as group means ± standard deviations for continuous variables. <italic>p</italic> values are derived from 1-way ANOVAs comparing all 4 groups (PD H1/H1, PD H2 carriers, control H1/H1, control H2 carriers); 2-tailed <italic>t</italic> tests comparing groups by <italic>MAPT</italic> haplotype and disease presence; and χ<sup>2</sup> tests for categorical variables. Results are presented without correction for multiple comparisons.</p><p>Key: ACE-R, Addenbrooke's Cognitive Examination (revised version); ANOVA, analysis of variance; BDI, Beck Depression Inventory; H&Y, Hoehn and Yahr; MDS-UPDRS 3, Movement Disorders Society Unified Parkinson's Disease Rating Scale Section <xref rid="sec3" ref-type="sec">3</xref> (motor features); NA, measure not applicable; NART, National Adult Reading Test; PD, Parkinson's disease.</p></fn></table-wrap-foot></table-wrap><table-wrap id="tbl2" position="float"><label>Table 2</label><caption><p>Activation differences associated with <italic>MAPT</italic> haplotype during memory task performance</p></caption><table frame="hsides" rules="groups"><thead><tr><th rowspan="2">Contrast</th><th rowspan="2">Contrast activation areas</th><th rowspan="2">Cluster size (voxels)</th><th colspan="3">Peak value coordinates<hr></hr></th></tr><tr><th>x</th><th>y</th><th>z</th></tr></thead><tbody><tr><td colspan="6">Contrast 1: successful encoding (remembered minus non-remembered)</td></tr><tr><td colspan="6"> All participants; H2 carriers > H1/H1</td></tr><tr><td> Cluster 1</td><td>L hippocampus, L parahippocampal gyrus, L amygdala, L fusiform gyrus, L inferior temporal gyrus</td><td align="char">927</td><td align="char">−36</td><td align="char">−34</td><td align="char">−8</td></tr><tr><td> Cluster 2</td><td>L Heschl's gyrus, L superior temporal gyrus, L middle temporal gyrus, L inferior temporal gyrus</td><td align="char">1687</td><td align="char">−48</td><td align="char">−48</td><td align="char">−4</td></tr><tr><td> Cluster 3</td><td>R hippocampus, R parahippocampal gyrus, R fusiform, R Heschl's gyrus, R superior temporal gyrus, R superior temporal pole, R middle temporal gyrus, R middle temporal pole, R inferior temporal gyrus</td><td align="char">2831</td><td align="char">42</td><td align="char">−18</td><td align="char">0</td></tr><tr><td colspan="6"> Patients with PD; H2 carriers > H1/H1</td></tr><tr><td> Cluster 1</td><td>L hippocampus, L parahippocampal gyrus, L amygdala, L fusiform gyrus, L inferior temporal gyrus</td><td align="char">619</td><td align="char">−36</td><td align="char">−32</td><td align="char">−10</td></tr><tr><td> Cluster 2</td><td>R hippocampus, R parahippocampal gyrus, R amygdala, R fusiform gyrus, R inferior temporal gyrus</td><td align="char">484</td><td align="char">44</td><td align="char">−16</td><td align="char">−24</td></tr><tr><td colspan="6"> Controls; H2 carriers > H1/H1</td></tr><tr><td> Cluster 1</td><td>L hippocampus, L parahippocampal gyrus, L fusiform gyrus</td><td align="char">230</td><td align="char">−30</td><td align="char">−34</td><td align="char">−26</td></tr><tr><td colspan="6">Contrast 2: overall task performance (all events minus baseline)</td></tr><tr><td colspan="6"> PD × MAPT interaction</td></tr><tr><td> Cluster 1</td><td>L hippocampus, L parahippocampal gyrus, L amygdala, L fusiform gyrus, L inferior temporal gyrus</td><td align="char">811</td><td align="char">−20</td><td align="char">−24</td><td align="char">−20</td></tr><tr><td> Cluster 2</td><td>R hippocampus, R parahippocampal gyrus, R amygdala, R fusiform gyrus, R inferior temporal gyrus</td><td align="char">259</td><td align="char">58</td><td align="char">−26</td><td align="char">−16</td></tr><tr><td colspan="6"> Patients with PD; H2 carriers > H1/H1</td></tr><tr><td> Cluster 1</td><td>L hippocampus, L parahippocampal gyrus, L fusiform gyrus, L superior temporal gyrus, L middle temporal gyrus, L inferior temporal gyrus</td><td align="char">2102</td><td align="char">−24</td><td align="char">−20</td><td align="char">−22</td></tr><tr><td> Cluster 2</td><td>R hippocampus, R parahippocampal gyrus, R fusiform gyrus, R superior temporal gyrus, R superior temporal pole, R middle temporal gyrus, R inferior temporal gyrus</td><td align="char">2316</td><td align="char">50</td><td align="char">−38</td><td align="char">−20</td></tr><tr><td colspan="6"> Controls; H2 carriers > H1/H1</td></tr><tr><td> Cluster 1</td><td>R superior temporal gyrus, R middle temporal gyrus</td><td align="char">582</td><td align="char">40</td><td align="char">−54</td><td align="char">10</td></tr></tbody></table><table-wrap-foot><fn><p>Details are provided for clusters of activation surviving cluster-based correction for multiple comparisons within an inclusive mask of the temporal lobes (<italic>p</italic> < 0.05 FWE corrected). There were no significant interactive effects of <italic>MAPT</italic> haplotype (H1 homozygotes vs. H2 carriers) and PD (patients vs. controls) for contrast 1 and no significant effect of <italic>MAPT</italic> haplotype (H2 carriers > H1/H1) across all participants for contrast 2. Coordinates listed are in Montreal Neurological Institute (MNI) standard space. Anatomic labels are derived from the AAL atlas.</p><p>Key: FWE, Family-wise error; L, left; PD, Parkinson's disease; R, right.</p></fn></table-wrap-foot></table-wrap></floats-group></pmc><affiliations><list><country><li>Canada</li><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Angleterre de l'Est</li><li>Grand Londres</li><li>Missouri (État)</li></region><settlement><li>Cambridge</li><li>Londres</li><li>Saint-Louis (Missouri)</li></settlement><orgName><li>Université Washington de Saint-Louis</li><li>Université de Cambridge</li></orgName></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Winder Rhodes, Sophie E" sort="Winder Rhodes, Sophie E" uniqKey="Winder Rhodes S" first="Sophie E." last="Winder-Rhodes">Sophie E. Winder-Rhodes</name></region><name sortKey="Barker, Roger A" sort="Barker, Roger A" uniqKey="Barker R" first="Roger A." last="Barker">Roger A. Barker</name><name sortKey="Barker, Roger A" sort="Barker, Roger A" uniqKey="Barker R" first="Roger A." last="Barker">Roger A. Barker</name><name sortKey="Hampshire, Adam" sort="Hampshire, Adam" uniqKey="Hampshire A" first="Adam" last="Hampshire">Adam Hampshire</name><name sortKey="Hampshire, Adam" sort="Hampshire, Adam" uniqKey="Hampshire A" first="Adam" last="Hampshire">Adam Hampshire</name><name sortKey="Owen, Adrian M" sort="Owen, Adrian M" uniqKey="Owen A" first="Adrian M." last="Owen">Adrian M. Owen</name><name sortKey="Robbins, Trevor W" sort="Robbins, Trevor W" uniqKey="Robbins T" first="Trevor W." last="Robbins">Trevor W. Robbins</name><name sortKey="Rowe, James B" sort="Rowe, James B" uniqKey="Rowe J" first="James B." last="Rowe">James B. Rowe</name><name sortKey="Rowe, James B" sort="Rowe, James B" uniqKey="Rowe J" first="James B." last="Rowe">James B. Rowe</name><name sortKey="Rowe, James B" sort="Rowe, James B" uniqKey="Rowe J" first="James B." last="Rowe">James B. Rowe</name><name sortKey="Winder Rhodes, Sophie E" sort="Winder Rhodes, Sophie E" uniqKey="Winder Rhodes S" first="Sophie E." last="Winder-Rhodes">Sophie E. Winder-Rhodes</name></country><country name="États-Unis"><region name="Missouri (État)"><name sortKey="Peelle, Jonathan E" sort="Peelle, Jonathan E" uniqKey="Peelle J" first="Jonathan E." last="Peelle">Jonathan E. Peelle</name></region></country><country name="Canada"><noRegion><name sortKey="Owen, Adrian M" sort="Owen, Adrian M" uniqKey="Owen A" first="Adrian M." last="Owen">Adrian M. Owen</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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