Genetic impact on cognition and brain function in newly diagnosed Parkinson's disease: ICICLE-PD study.
Identifieur interne : 000667 ( PubMed/Curation ); précédent : 000666; suivant : 000668Genetic impact on cognition and brain function in newly diagnosed Parkinson's disease: ICICLE-PD study.
Auteurs : Cristina Nombela [Oman] ; James B. Rowe [Royaume-Uni] ; Sophie E. Winder-Rhodes [Royaume-Uni] ; Adam Hampshire [Royaume-Uni] ; Adrian M. Owen [Canada] ; David P. Breen [Royaume-Uni] ; Gordon W. Duncan [Royaume-Uni] ; Tien K. Khoo [Australie] ; Alison J. Yarnall [Royaume-Uni] ; Michael J. Firbank [Royaume-Uni] ; Patrick F. Chinnery [Royaume-Uni] ; Trevor W. Robbins [Royaume-Uni] ; John T. O'Brien [Royaume-Uni] ; David J. Brooks [Danemark] ; David J. Burn [Royaume-Uni] ; Roger A. Barker [Royaume-Uni]Source :
- Brain : a journal of neurology [ 1460-2156 ] ; 2014.
English descriptors
- KwdEn :
- Aged, Apolipoproteins E (genetics), Brain (physiopathology), Catechol O-Methyltransferase (genetics), Cognition (physiology), Cognition Disorders (etiology), Cognition Disorders (psychology), Cohort Studies, Female, Humans, Image Processing, Computer-Assisted, Imagination (physiology), Longitudinal Studies, Magnetic Resonance Imaging, Male, Memory (physiology), Middle Aged, Mitogen-Activated Protein Kinases (genetics), Neuroimaging, Neuropsychological Tests, Parkinson Disease (genetics), Parkinson Disease (physiopathology), Psychomotor Performance (physiology), Rotation, Space Perception (physiology), tau Proteins (genetics).
- MESH :
- chemical , genetics : Apolipoproteins E, Catechol O-Methyltransferase, Mitogen-Activated Protein Kinases, tau Proteins.
- etiology : Cognition Disorders.
- genetics : Parkinson Disease.
- physiology : Cognition, Imagination, Memory, Psychomotor Performance, Space Perception.
- physiopathology : Brain, Parkinson Disease.
- psychology : Cognition Disorders.
- Aged, Cohort Studies, Female, Humans, Image Processing, Computer-Assisted, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Neuroimaging, Neuropsychological Tests, Rotation.
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.
DOI: 10.1093/brain/awu201
PubMed: 25080285
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Rowe</name><affiliation wicri:level="1"><nlm:affiliation>2 Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK 3 Medical Research Council, Cognition and Brain Sciences Unit, Cambridge, UK 4 Behavioural and Clinical Neuroscience Institute, University of Cambridge, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>2 Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK 3 Medical Research Council, Cognition and Brain Sciences Unit, Cambridge, UK 4 Behavioural and Clinical Neuroscience Institute, University of Cambridge</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>1 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>1 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge</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>5 Computational, Cognitive and Clinical Neuroscience Laboratory, Imperial College London, London, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>5 Computational, Cognitive and Clinical Neuroscience Laboratory, Imperial College London, London</wicri:regionArea></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:affiliation>6 Brain and Mind Institute, University of Western Ontario, London, Canada 7 Department of Psychology, University of Western Ontario, London, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>6 Brain and Mind Institute, University of Western Ontario, London, Canada 7 Department of Psychology, University of Western Ontario, London</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>1 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>1 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>8 Institute for Ageing and Health, Newcastle University, Newcastle, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>8 Institute for Ageing and Health, Newcastle University, Newcastle</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>9 Griffith Health Institute and School of Medicine, Griffith University, Gold Coast, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>9 Griffith Health Institute and School of Medicine, Griffith University, Gold Coast</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>8 Institute for Ageing and Health, Newcastle University, Newcastle, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>8 Institute for Ageing and Health, Newcastle University, Newcastle</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>8 Institute for Ageing and Health, Newcastle University, Newcastle, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>8 Institute for Ageing and Health, Newcastle University, Newcastle</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>10 Institute of Genetic Medicine, Newcastle University, Newcastle, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>10 Institute of Genetic Medicine, Newcastle University, Newcastle</wicri:regionArea></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="1"><nlm:affiliation>4 Behavioural and Clinical Neuroscience Institute, University of Cambridge, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>4 Behavioural and Clinical Neuroscience Institute, University of Cambridge</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>11 Department of Psychiatry, University of Cambridge, Cambridge, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>11 Department of Psychiatry, University of Cambridge, Cambridge</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>12 Imperial College London, London, UK 13 Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University, Denmark.</nlm:affiliation><country xml:lang="fr">Danemark</country><wicri:regionArea>12 Imperial College London, London, UK 13 Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>8 Institute for Ageing and Health, Newcastle University, Newcastle, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>8 Institute for Ageing and Health, Newcastle University, Newcastle</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>1 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>1 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge</wicri:regionArea></affiliation></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>Apolipoproteins E (genetics)</term><term>Brain (physiopathology)</term><term>Catechol O-Methyltransferase (genetics)</term><term>Cognition (physiology)</term><term>Cognition Disorders (etiology)</term><term>Cognition Disorders (psychology)</term><term>Cohort Studies</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Imagination (physiology)</term><term>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Memory (physiology)</term><term>Middle Aged</term><term>Mitogen-Activated Protein Kinases (genetics)</term><term>Neuroimaging</term><term>Neuropsychological Tests</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (physiopathology)</term><term>Psychomotor Performance (physiology)</term><term>Rotation</term><term>Space Perception (physiology)</term><term>tau Proteins (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Apolipoproteins E</term><term>Catechol O-Methyltransferase</term><term>Mitogen-Activated Protein Kinases</term><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cognition</term><term>Imagination</term><term>Memory</term><term>Psychomotor Performance</term><term>Space Perception</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Cohort Studies</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Neuroimaging</term><term>Neuropsychological Tests</term><term>Rotation</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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25080285</PMID><DateCreated><Year>2014</Year><Month>09</Month><Day>14</Day></DateCreated><DateCompleted><Year>2014</Year><Month>11</Month><Day>04</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 10</Issue><PubDate><Year>2014</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Genetic impact on cognition and brain function in newly diagnosed Parkinson's disease: ICICLE-PD study.</ArticleTitle><Pagination><MedlinePgn>2743-58</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/brain/awu201</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>© The Author (2014). Published by Oxford University Press on behalf of the Guarantors of Brain.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nombela</LastName><ForeName>Cristina</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>1 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK dra.cristinanombela@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rowe</LastName><ForeName>James B</ForeName><Initials>JB</Initials><AffiliationInfo><Affiliation>2 Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK 3 Medical Research Council, Cognition and Brain Sciences Unit, Cambridge, UK 4 Behavioural and Clinical Neuroscience Institute, University of Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Winder-Rhodes</LastName><ForeName>Sophie E</ForeName><Initials>SE</Initials><AffiliationInfo><Affiliation>1 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hampshire</LastName><ForeName>Adam</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>5 Computational, Cognitive and Clinical Neuroscience Laboratory, Imperial College London, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Owen</LastName><ForeName>Adrian M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>6 Brain and Mind Institute, University of Western Ontario, London, Canada 7 Department of Psychology, University of Western Ontario, London, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Breen</LastName><ForeName>David P</ForeName><Initials>DP</Initials><AffiliationInfo><Affiliation>1 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Duncan</LastName><ForeName>Gordon W</ForeName><Initials>GW</Initials><AffiliationInfo><Affiliation>8 Institute for Ageing and Health, Newcastle University, Newcastle, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khoo</LastName><ForeName>Tien K</ForeName><Initials>TK</Initials><AffiliationInfo><Affiliation>9 Griffith Health Institute and School of Medicine, Griffith University, Gold Coast, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yarnall</LastName><ForeName>Alison J</ForeName><Initials>AJ</Initials><AffiliationInfo><Affiliation>8 Institute for Ageing and Health, Newcastle University, Newcastle, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Firbank</LastName><ForeName>Michael J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>8 Institute for Ageing and Health, Newcastle University, Newcastle, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chinnery</LastName><ForeName>Patrick F</ForeName><Initials>PF</Initials><AffiliationInfo><Affiliation>10 Institute of Genetic Medicine, Newcastle University, Newcastle, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Robbins</LastName><ForeName>Trevor W</ForeName><Initials>TW</Initials><AffiliationInfo><Affiliation>4 Behavioural and Clinical Neuroscience Institute, University of Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>O'Brien</LastName><ForeName>John T</ForeName><Initials>JT</Initials><AffiliationInfo><Affiliation>11 Department of Psychiatry, University of Cambridge, Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brooks</LastName><ForeName>David J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>12 Imperial College London, London, UK 13 Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Burn</LastName><ForeName>David J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>8 Institute for Ageing and Health, Newcastle University, Newcastle, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><CollectiveName>ICICLE-PD study group</CollectiveName></Author><Author ValidYN="Y"><LastName>Barker</LastName><ForeName>Roger A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>1 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>G1100810</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>G0001354</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>101876</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>G-1301</GrantID><Agency>Parkinson's UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>MC_U120036861</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>MR/K000608/1</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><GrantID>J-0802</GrantID><Agency>Parkinson's UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>088324</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>JBR 088324</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>07</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001057">Apolipoproteins E</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.1.1.6</RegistryNumber><NameOfSubstance UI="D002394">Catechol O-Methyltransferase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D020928">Mitogen-Activated Protein 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