Genetic impact on cognition and brain function in newly diagnosed Parkinson's disease: ICICLE-PD study
Identifieur interne : 000010 ( PascalFrancis/Corpus ); précédent : 000009; suivant : 000011Genetic impact on cognition and brain function in newly diagnosed Parkinson's disease: ICICLE-PD study
Auteurs : Cristina Nombela ; James B. Rowe ; Sophie E. Winder-Rhodes ; Adam Hampshire ; Adrian M. Owen ; David P. Breen ; Gordon W. Duncan ; Tien K. Khoo ; Alison J. Yarnall ; Michael J. Firbank ; Patrick F. Chinnery ; Trevor W. Robbins ; John T. O'Brien ; David J. Brooks ; David J. Burn ; Roger A. BarkerSource :
- Brain [ 0006-8950 ] ; 2014.
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- Pascal (Inist)
English descriptors
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Abstract
Parkinson's disease is associated with multiple cognitive impairments and increased risk of dementia, but the extent of these deficits varies widely among patients. The ICICLE-PD study was established to define the characteristics and prevalence of cognitive change soon after diagnosis, in a representative cohort of patients, using a multimodal approach. Specifically, we tested the 'Dual Syndrome' hypothesis for cognitive impairment in Parkinson's disease, which distinguishes an executive syndrome (affecting the frontostriatal regions due to dopaminergic deficits) from a posterior cortical syndrome (affecting visuospatial, mnemonic and semantic functions related to Lewy body pathology and secondary cholinergic loss). An incident Parkinson's disease cohort (n = 168, median 8 months from diagnosis to participation) and matched control group (n = 85) were recruited to a neuroimaging study at two sites in the UK. All participants underwent clinical, neuropsychological and functional magnetic resonance imaging assessments. The three neuroimaging tasks (Tower of London, Spatial Rotations and Memory Encoding Tasks) were designed to probe executive, visuospatial and memory encoding domains, respectively. Patients were also genotyped for three polymorphisms associated with cognitive change in Parkinson's disease and related disorders: (i) rs4680 for COMT Val158Met polymorphism; (ii) rs9468 for MAPT H1 versus H2 haplotype; and (iii) rs429358 for APOE-ε2, 3, 4. We identified performance deficits in all three cognitive domains, which were associated with regionally specific changes in cortical activation. Task-specific regional activations in Parkinson's disease were linked with genetic variation: the rs4680 polymorphism modulated the effect of levodopa therapy on planning-related activations in the frontoparietal network; the MAPT haplotype modulated parietal activations associated with spatial rotations; and APOE allelic variation influenced the magnitude of activation associated with memory encoding. This study demonstrates that neurocognitive deficits are common even in recently diagnosed patients with Parkinson's disease, and that the associated regional brain activations are influenced by genotype. These data further support the dual syndrome hypothesis of cognitive change in Parkinson's disease. Longitudinal data will confirm the extent to which these early neurocognitive changes, and their genetic factors, influence the long-term risk of dementia in Parkinson's disease. The combination of genetics and functional neuroimaging provides a potentially useful method for stratification and identification of candidate markers, in future clinical trials against cognitive decline in Parkinson's disease.
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| NO : | PASCAL 14-0238595 INIST |
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| ET : | Genetic impact on cognition and brain function in newly diagnosed Parkinson's disease: ICICLE-PD study |
| AU : | NOMBELA (Cristina); ROWE (James B.); WINDER-RHODES (Sophie E.); HAMPSHIRE (Adam); OWEN (Adrian M.); BREEN (David P.); DUNCAN (Gordon W.); KHOO (Tien K.); YARNALL (Alison J.); FIRBANK (Michael J.); CHINNERY (Patrick F.); ROBBINS (Trevor W.); O'BRIEN (John T.); BROOKS (David J.); BURN (David J.); BARKER (Roger A.) |
| AF : | John van Geest Centre for Brain Repair, University of Cambridge/Cambridge/Royaume-Uni (1 aut., 3 aut., 6 aut., 16 aut.); Department of Clinical Neurosciences, University of Cambridge/Cambridge/Royaume-Uni (2 aut.); Medical Research Council, Cognition and Brain Sciences Unit/Cambridge/Royaume-Uni (2 aut.); Behavioural and Clinical Neuroscience Institute, University of Cambridge/Royaume-Uni (2 aut., 12 aut.); Computational, Cognitive and Clinical Neuroscience Laboratory, Imperial College London/London/Royaume-Uni (4 aut.); Brain and Mind Institute, University of Western Ontario/London/Canada (5 aut.); Department of Psychology, University of Western Ontario/London/Canada (5 aut.); Institute for Ageing and Health, Newcastle University/Newcastle/Royaume-Uni (7 aut., 9 aut., 10 aut., 15 aut.); Griffith Health Institute and School of Medicine, Griffith University/Gold Coast/Australie (8 aut.); Institute of Genetic Medicine, Newcastle University/Newcastle/Royaume-Uni (11 aut.); Department of Psychiatry, University of Cambridge/Cambridge/Royaume-Uni (13 aut.); Imperial College London/London/Royaume-Uni (14 aut.); Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University/Danemark (14 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Brain; ISSN 0006-8950; Royaume-Uni; Da. 2014; Vol. 137; No. p. 10; Pp. 2743-2758; Bibl. 2 p.1/4 |
| LA : | Anglais |
| EA : | Parkinson's disease is associated with multiple cognitive impairments and increased risk of dementia, but the extent of these deficits varies widely among patients. The ICICLE-PD study was established to define the characteristics and prevalence of cognitive change soon after diagnosis, in a representative cohort of patients, using a multimodal approach. Specifically, we tested the 'Dual Syndrome' hypothesis for cognitive impairment in Parkinson's disease, which distinguishes an executive syndrome (affecting the frontostriatal regions due to dopaminergic deficits) from a posterior cortical syndrome (affecting visuospatial, mnemonic and semantic functions related to Lewy body pathology and secondary cholinergic loss). An incident Parkinson's disease cohort (n = 168, median 8 months from diagnosis to participation) and matched control group (n = 85) were recruited to a neuroimaging study at two sites in the UK. All participants underwent clinical, neuropsychological and functional magnetic resonance imaging assessments. The three neuroimaging tasks (Tower of London, Spatial Rotations and Memory Encoding Tasks) were designed to probe executive, visuospatial and memory encoding domains, respectively. Patients were also genotyped for three polymorphisms associated with cognitive change in Parkinson's disease and related disorders: (i) rs4680 for COMT Val158Met polymorphism; (ii) rs9468 for MAPT H1 versus H2 haplotype; and (iii) rs429358 for APOE-ε2, 3, 4. We identified performance deficits in all three cognitive domains, which were associated with regionally specific changes in cortical activation. Task-specific regional activations in Parkinson's disease were linked with genetic variation: the rs4680 polymorphism modulated the effect of levodopa therapy on planning-related activations in the frontoparietal network; the MAPT haplotype modulated parietal activations associated with spatial rotations; and APOE allelic variation influenced the magnitude of activation associated with memory encoding. This study demonstrates that neurocognitive deficits are common even in recently diagnosed patients with Parkinson's disease, and that the associated regional brain activations are influenced by genotype. These data further support the dual syndrome hypothesis of cognitive change in Parkinson's disease. Longitudinal data will confirm the extent to which these early neurocognitive changes, and their genetic factors, influence the long-term risk of dementia in Parkinson's disease. The combination of genetics and functional neuroimaging provides a potentially useful method for stratification and identification of candidate markers, in future clinical trials against cognitive decline in Parkinson's disease. |
| CC : | 002B17G; 002B17A01; 002B17A03 |
| FD : | Maladie de Parkinson; Pathologie du système nerveux; Cognition; Encéphale; Imagerie RMN |
| FG : | Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central; Imagerie médicale |
| ED : | Parkinson disease; Nervous system diseases; Cognition; Encephalon; Nuclear magnetic resonance imaging |
| EG : | Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Medical imagery |
| SD : | Parkinson enfermedad; Sistema nervioso patología; Cognición; Encéfalo; Imaginería RMN |
| LO : | INIST-998.354000502618830160 |
| ID : | 14-0238595 |
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Brooks</name><affiliation><inist:fA14 i1="12"><s1>Imperial College London</s1><s2>London</s2><s3>GBR</s3><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="13"><s1>Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University</s1><s3>DNK</s3><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Burn, David J" sort="Burn, David J" uniqKey="Burn D" first="David J." last="Burn">David J. Burn</name><affiliation><inist:fA14 i1="08"><s1>Institute for Ageing and Health, Newcastle University</s1><s2>Newcastle</s2><s3>GBR</s3><sZ>7 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></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><inist:fA14 i1="01"><s1>John van Geest Centre for Brain Repair, University of Cambridge</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>16 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">14-0238595</idno><date when="2014">2014</date><idno type="stanalyst">PASCAL 14-0238595 INIST</idno><idno type="RBID">Pascal:14-0238595</idno><idno type="wicri:Area/PascalFrancis/Corpus">000010</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Genetic impact on cognition and brain function in newly diagnosed Parkinson's disease: ICICLE-PD study</title><author><name sortKey="Nombela, Cristina" sort="Nombela, Cristina" uniqKey="Nombela C" first="Cristina" last="Nombela">Cristina Nombela</name><affiliation><inist:fA14 i1="01"><s1>John van Geest Centre for Brain Repair, University of Cambridge</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>16 aut.</sZ></inist:fA14></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><inist:fA14 i1="02"><s1>Department of Clinical Neurosciences, University of Cambridge</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>2 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Medical Research Council, Cognition and Brain Sciences Unit</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>2 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Behavioural and Clinical Neuroscience Institute, University of Cambridge</s1><s3>GBR</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><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><affiliation><inist:fA14 i1="01"><s1>John van Geest Centre for Brain Repair, University of Cambridge</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>16 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Hampshire, Adam" sort="Hampshire, Adam" uniqKey="Hampshire A" first="Adam" last="Hampshire">Adam Hampshire</name><affiliation><inist:fA14 i1="05"><s1>Computational, Cognitive and Clinical Neuroscience Laboratory, Imperial College London</s1><s2>London</s2><s3>GBR</s3><sZ>4 aut.</sZ></inist:fA14></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><inist:fA14 i1="06"><s1>Brain and Mind Institute, University of Western Ontario</s1><s2>London</s2><s3>CAN</s3><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="07"><s1>Department of Psychology, University of Western Ontario</s1><s2>London</s2><s3>CAN</s3><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Breen, David P" sort="Breen, David P" uniqKey="Breen D" first="David P." last="Breen">David P. Breen</name><affiliation><inist:fA14 i1="01"><s1>John van Geest Centre for Brain Repair, University of Cambridge</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>16 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Duncan, Gordon W" sort="Duncan, Gordon W" uniqKey="Duncan G" first="Gordon W." last="Duncan">Gordon W. Duncan</name><affiliation><inist:fA14 i1="08"><s1>Institute for Ageing and Health, Newcastle University</s1><s2>Newcastle</s2><s3>GBR</s3><sZ>7 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Khoo, Tien K" sort="Khoo, Tien K" uniqKey="Khoo T" first="Tien K." last="Khoo">Tien K. Khoo</name><affiliation><inist:fA14 i1="09"><s1>Griffith Health Institute and School of Medicine, Griffith University</s1><s2>Gold Coast</s2><s3>AUS</s3><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Yarnall, Alison J" sort="Yarnall, Alison J" uniqKey="Yarnall A" first="Alison J." last="Yarnall">Alison J. Yarnall</name><affiliation><inist:fA14 i1="08"><s1>Institute for Ageing and Health, Newcastle University</s1><s2>Newcastle</s2><s3>GBR</s3><sZ>7 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Firbank, Michael J" sort="Firbank, Michael J" uniqKey="Firbank M" first="Michael J." last="Firbank">Michael J. Firbank</name><affiliation><inist:fA14 i1="08"><s1>Institute for Ageing and Health, Newcastle University</s1><s2>Newcastle</s2><s3>GBR</s3><sZ>7 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Chinnery, Patrick F" sort="Chinnery, Patrick F" uniqKey="Chinnery P" first="Patrick F." last="Chinnery">Patrick F. Chinnery</name><affiliation><inist:fA14 i1="10"><s1>Institute of Genetic Medicine, Newcastle University</s1><s2>Newcastle</s2><s3>GBR</s3><sZ>11 aut.</sZ></inist:fA14></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><inist:fA14 i1="04"><s1>Behavioural and Clinical Neuroscience Institute, University of Cambridge</s1><s3>GBR</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="O Brien, John T" sort="O Brien, John T" uniqKey="O Brien J" first="John T." last="O'Brien">John T. O'Brien</name><affiliation><inist:fA14 i1="11"><s1>Department of Psychiatry, University of Cambridge</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name><affiliation><inist:fA14 i1="12"><s1>Imperial College London</s1><s2>London</s2><s3>GBR</s3><sZ>14 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="13"><s1>Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University</s1><s3>DNK</s3><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Burn, David J" sort="Burn, David J" uniqKey="Burn D" first="David J." last="Burn">David J. Burn</name><affiliation><inist:fA14 i1="08"><s1>Institute for Ageing and Health, Newcastle University</s1><s2>Newcastle</s2><s3>GBR</s3><sZ>7 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></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><inist:fA14 i1="01"><s1>John van Geest Centre for Brain Repair, University of Cambridge</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>16 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Brain</title><title level="j" type="abbreviated">Brain</title><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cognition</term><term>Encephalon</term><term>Nervous system diseases</term><term>Nuclear magnetic resonance imaging</term><term>Parkinson disease</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Cognition</term><term>Encéphale</term><term>Imagerie RMN</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is associated with multiple cognitive impairments and increased risk of dementia, but the extent of these deficits varies widely among patients. The ICICLE-PD study was established to define the characteristics and prevalence of cognitive change soon after diagnosis, in a representative cohort of patients, using a multimodal approach. Specifically, we tested the 'Dual Syndrome' hypothesis for cognitive impairment in Parkinson's disease, which distinguishes an executive syndrome (affecting the frontostriatal regions due to dopaminergic deficits) from a posterior cortical syndrome (affecting visuospatial, mnemonic and semantic functions related to Lewy body pathology and secondary cholinergic loss). An incident Parkinson's disease cohort (n = 168, median 8 months from diagnosis to participation) and matched control group (n = 85) were recruited to a neuroimaging study at two sites in the UK. All participants underwent clinical, neuropsychological and functional magnetic resonance imaging assessments. The three neuroimaging tasks (Tower of London, Spatial Rotations and Memory Encoding Tasks) were designed to probe executive, visuospatial and memory encoding domains, respectively. Patients were also genotyped for three polymorphisms associated with cognitive change in Parkinson's disease and related disorders: (i) rs4680 for COMT Val158Met polymorphism; (ii) rs9468 for MAPT H1 versus H2 haplotype; and (iii) rs429358 for APOE-ε2, 3, 4. We identified performance deficits in all three cognitive domains, which were associated with regionally specific changes in cortical activation. Task-specific regional activations in Parkinson's disease were linked with genetic variation: the rs4680 polymorphism modulated the effect of levodopa therapy on planning-related activations in the frontoparietal network; the MAPT haplotype modulated parietal activations associated with spatial rotations; and APOE allelic variation influenced the magnitude of activation associated with memory encoding. This study demonstrates that neurocognitive deficits are common even in recently diagnosed patients with Parkinson's disease, and that the associated regional brain activations are influenced by genotype. These data further support the dual syndrome hypothesis of cognitive change in Parkinson's disease. Longitudinal data will confirm the extent to which these early neurocognitive changes, and their genetic factors, influence the long-term risk of dementia in Parkinson's disease. The combination of genetics and functional neuroimaging provides a potentially useful method for stratification and identification of candidate markers, in future clinical trials against cognitive decline in Parkinson's disease.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0006-8950</s0></fA01><fA03 i2="1"><s0>Brain</s0></fA03><fA05><s2>137</s2></fA05><fA06><s3>p. 10</s3></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Genetic impact on cognition and brain function in newly diagnosed Parkinson's disease: ICICLE-PD study</s1></fA08><fA11 i1="01" i2="1"><s1>NOMBELA (Cristina)</s1></fA11><fA11 i1="02" i2="1"><s1>ROWE (James B.)</s1></fA11><fA11 i1="03" i2="1"><s1>WINDER-RHODES (Sophie E.)</s1></fA11><fA11 i1="04" i2="1"><s1>HAMPSHIRE (Adam)</s1></fA11><fA11 i1="05" i2="1"><s1>OWEN (Adrian M.)</s1></fA11><fA11 i1="06" i2="1"><s1>BREEN (David P.)</s1></fA11><fA11 i1="07" i2="1"><s1>DUNCAN (Gordon W.)</s1></fA11><fA11 i1="08" i2="1"><s1>KHOO (Tien K.)</s1></fA11><fA11 i1="09" i2="1"><s1>YARNALL (Alison J.)</s1></fA11><fA11 i1="10" i2="1"><s1>FIRBANK (Michael J.)</s1></fA11><fA11 i1="11" i2="1"><s1>CHINNERY (Patrick F.)</s1></fA11><fA11 i1="12" i2="1"><s1>ROBBINS (Trevor W.)</s1></fA11><fA11 i1="13" i2="1"><s1>O'BRIEN (John T.)</s1></fA11><fA11 i1="14" i2="1"><s1>BROOKS (David J.)</s1></fA11><fA11 i1="15" i2="1"><s1>BURN (David J.)</s1></fA11><fA11 i1="16" i2="1"><s1>BARKER (Roger A.)</s1></fA11><fA14 i1="01"><s1>John van Geest Centre for Brain Repair, University of Cambridge</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ><sZ>16 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Clinical Neurosciences, University of Cambridge</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>2 aut.</sZ></fA14><fA14 i1="03"><s1>Medical Research Council, Cognition and Brain Sciences Unit</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>2 aut.</sZ></fA14><fA14 i1="04"><s1>Behavioural and Clinical Neuroscience Institute, University of Cambridge</s1><s3>GBR</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ></fA14><fA14 i1="05"><s1>Computational, Cognitive and Clinical Neuroscience Laboratory, Imperial College London</s1><s2>London</s2><s3>GBR</s3><sZ>4 aut.</sZ></fA14><fA14 i1="06"><s1>Brain and Mind Institute, University of Western Ontario</s1><s2>London</s2><s3>CAN</s3><sZ>5 aut.</sZ></fA14><fA14 i1="07"><s1>Department of Psychology, University of Western Ontario</s1><s2>London</s2><s3>CAN</s3><sZ>5 aut.</sZ></fA14><fA14 i1="08"><s1>Institute for Ageing and Health, Newcastle University</s1><s2>Newcastle</s2><s3>GBR</s3><sZ>7 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ><sZ>15 aut.</sZ></fA14><fA14 i1="09"><s1>Griffith Health Institute and School of Medicine, Griffith University</s1><s2>Gold Coast</s2><s3>AUS</s3><sZ>8 aut.</sZ></fA14><fA14 i1="10"><s1>Institute of Genetic Medicine, Newcastle University</s1><s2>Newcastle</s2><s3>GBR</s3><sZ>11 aut.</sZ></fA14><fA14 i1="11"><s1>Department of Psychiatry, University of Cambridge</s1><s2>Cambridge</s2><s3>GBR</s3><sZ>13 aut.</sZ></fA14><fA14 i1="12"><s1>Imperial College London</s1><s2>London</s2><s3>GBR</s3><sZ>14 aut.</sZ></fA14><fA14 i1="13"><s1>Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University</s1><s3>DNK</s3><sZ>14 aut.</sZ></fA14><fA17 i1="01" i2="1"><s1>ICICLE-PD study group</s1><s3>INC</s3></fA17><fA20><s1>2743-2758</s1></fA20><fA21><s1>2014</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>998</s2><s5>354000502618830160</s5></fA43><fA44><s0>0000</s0><s1>© 2014 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>2 p.1/4</s0></fA45><fA47 i1="01" i2="1"><s0>14-0238595</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Brain</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>Parkinson's disease is associated with multiple cognitive impairments and increased risk of dementia, but the extent of these deficits varies widely among patients. The ICICLE-PD study was established to define the characteristics and prevalence of cognitive change soon after diagnosis, in a representative cohort of patients, using a multimodal approach. Specifically, we tested the 'Dual Syndrome' hypothesis for cognitive impairment in Parkinson's disease, which distinguishes an executive syndrome (affecting the frontostriatal regions due to dopaminergic deficits) from a posterior cortical syndrome (affecting visuospatial, mnemonic and semantic functions related to Lewy body pathology and secondary cholinergic loss). An incident Parkinson's disease cohort (n = 168, median 8 months from diagnosis to participation) and matched control group (n = 85) were recruited to a neuroimaging study at two sites in the UK. All participants underwent clinical, neuropsychological and functional magnetic resonance imaging assessments. The three neuroimaging tasks (Tower of London, Spatial Rotations and Memory Encoding Tasks) were designed to probe executive, visuospatial and memory encoding domains, respectively. Patients were also genotyped for three polymorphisms associated with cognitive change in Parkinson's disease and related disorders: (i) rs4680 for COMT Val158Met polymorphism; (ii) rs9468 for MAPT H1 versus H2 haplotype; and (iii) rs429358 for APOE-ε2, 3, 4. We identified performance deficits in all three cognitive domains, which were associated with regionally specific changes in cortical activation. Task-specific regional activations in Parkinson's disease were linked with genetic variation: the rs4680 polymorphism modulated the effect of levodopa therapy on planning-related activations in the frontoparietal network; the MAPT haplotype modulated parietal activations associated with spatial rotations; and APOE allelic variation influenced the magnitude of activation associated with memory encoding. This study demonstrates that neurocognitive deficits are common even in recently diagnosed patients with Parkinson's disease, and that the associated regional brain activations are influenced by genotype. These data further support the dual syndrome hypothesis of cognitive change in Parkinson's disease. Longitudinal data will confirm the extent to which these early neurocognitive changes, and their genetic factors, influence the long-term risk of dementia in Parkinson's disease. The combination of genetics and functional neuroimaging provides a potentially useful method for stratification and identification of candidate markers, in future clinical trials against cognitive decline in Parkinson's disease.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC02 i1="02" i2="X"><s0>002B17A01</s0></fC02><fC02 i1="03" i2="X"><s0>002B17A03</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Maladie de Parkinson</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Cognition</s0><s5>09</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Cognition</s0><s5>09</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Cognición</s0><s5>09</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Encéphale</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Encephalon</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Encéfalo</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Imagerie RMN</s0><s5>11</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Nuclear magnetic resonance imaging</s0><s5>11</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Imaginería RMN</s0><s5>11</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Central nervous system</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>41</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>41</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Imagerie médicale</s0><s5>43</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Medical imagery</s0><s5>43</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Imaginería médica</s0><s5>43</s5></fC07><fN21><s1>286</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 14-0238595 INIST</NO><ET>Genetic impact on cognition and brain function in newly diagnosed Parkinson's disease: ICICLE-PD study</ET><AU>NOMBELA (Cristina); ROWE (James B.); WINDER-RHODES (Sophie E.); HAMPSHIRE (Adam); OWEN (Adrian M.); BREEN (David P.); DUNCAN (Gordon W.); KHOO (Tien K.); YARNALL (Alison J.); FIRBANK (Michael J.); CHINNERY (Patrick F.); ROBBINS (Trevor W.); O'BRIEN (John T.); BROOKS (David J.); BURN (David J.); BARKER (Roger A.)</AU><AF>John van Geest Centre for Brain Repair, University of Cambridge/Cambridge/Royaume-Uni (1 aut., 3 aut., 6 aut., 16 aut.); Department of Clinical Neurosciences, University of Cambridge/Cambridge/Royaume-Uni (2 aut.); Medical Research Council, Cognition and Brain Sciences Unit/Cambridge/Royaume-Uni (2 aut.); Behavioural and Clinical Neuroscience Institute, University of Cambridge/Royaume-Uni (2 aut., 12 aut.); Computational, Cognitive and Clinical Neuroscience Laboratory, Imperial College London/London/Royaume-Uni (4 aut.); Brain and Mind Institute, University of Western Ontario/London/Canada (5 aut.); Department of Psychology, University of Western Ontario/London/Canada (5 aut.); Institute for Ageing and Health, Newcastle University/Newcastle/Royaume-Uni (7 aut., 9 aut., 10 aut., 15 aut.); Griffith Health Institute and School of Medicine, Griffith University/Gold Coast/Australie (8 aut.); Institute of Genetic Medicine, Newcastle University/Newcastle/Royaume-Uni (11 aut.); Department of Psychiatry, University of Cambridge/Cambridge/Royaume-Uni (13 aut.); Imperial College London/London/Royaume-Uni (14 aut.); Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University/Danemark (14 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Brain; ISSN 0006-8950; Royaume-Uni; Da. 2014; Vol. 137; No. p. 10; Pp. 2743-2758; Bibl. 2 p.1/4</SO><LA>Anglais</LA><EA>Parkinson's disease is associated with multiple cognitive impairments and increased risk of dementia, but the extent of these deficits varies widely among patients. The ICICLE-PD study was established to define the characteristics and prevalence of cognitive change soon after diagnosis, in a representative cohort of patients, using a multimodal approach. Specifically, we tested the 'Dual Syndrome' hypothesis for cognitive impairment in Parkinson's disease, which distinguishes an executive syndrome (affecting the frontostriatal regions due to dopaminergic deficits) from a posterior cortical syndrome (affecting visuospatial, mnemonic and semantic functions related to Lewy body pathology and secondary cholinergic loss). An incident Parkinson's disease cohort (n = 168, median 8 months from diagnosis to participation) and matched control group (n = 85) were recruited to a neuroimaging study at two sites in the UK. All participants underwent clinical, neuropsychological and functional magnetic resonance imaging assessments. The three neuroimaging tasks (Tower of London, Spatial Rotations and Memory Encoding Tasks) were designed to probe executive, visuospatial and memory encoding domains, respectively. Patients were also genotyped for three polymorphisms associated with cognitive change in Parkinson's disease and related disorders: (i) rs4680 for COMT Val158Met polymorphism; (ii) rs9468 for MAPT H1 versus H2 haplotype; and (iii) rs429358 for APOE-ε2, 3, 4. We identified performance deficits in all three cognitive domains, which were associated with regionally specific changes in cortical activation. Task-specific regional activations in Parkinson's disease were linked with genetic variation: the rs4680 polymorphism modulated the effect of levodopa therapy on planning-related activations in the frontoparietal network; the MAPT haplotype modulated parietal activations associated with spatial rotations; and APOE allelic variation influenced the magnitude of activation associated with memory encoding. This study demonstrates that neurocognitive deficits are common even in recently diagnosed patients with Parkinson's disease, and that the associated regional brain activations are influenced by genotype. These data further support the dual syndrome hypothesis of cognitive change in Parkinson's disease. Longitudinal data will confirm the extent to which these early neurocognitive changes, and their genetic factors, influence the long-term risk of dementia in Parkinson's disease. The combination of genetics and functional neuroimaging provides a potentially useful method for stratification and identification of candidate markers, in future clinical trials against cognitive decline in Parkinson's disease.</EA><CC>002B17G; 002B17A01; 002B17A03</CC><FD>Maladie de Parkinson; Pathologie du système nerveux; Cognition; Encéphale; Imagerie RMN</FD><FG>Système nerveux central; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central; Imagerie médicale</FG><ED>Parkinson disease; Nervous system diseases; Cognition; Encephalon; Nuclear magnetic resonance imaging</ED><EG>Central nervous system; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Medical imagery</EG><SD>Parkinson enfermedad; Sistema nervioso patología; Cognición; Encéfalo; Imaginería RMN</SD><LO>INIST-998.354000502618830160</LO><ID>14-0238595</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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