Baseline and longitudinal grey matter changes in newly diagnosed Parkinson's disease: ICICLE-PD study.
Identifieur interne : 000390 ( PubMed/Curation ); précédent : 000389; suivant : 000391Baseline and longitudinal grey matter changes in newly diagnosed Parkinson's disease: ICICLE-PD study.
Auteurs : Elijah Mak [Royaume-Uni] ; Li Su [Royaume-Uni] ; Guy B. Williams [Royaume-Uni] ; Michael J. Firbank [Royaume-Uni] ; Rachael A. Lawson [Royaume-Uni] ; Alison J. Yarnall [Royaume-Uni] ; Gordon W. Duncan [Royaume-Uni] ; Adrian M. Owen [Canada] ; Tien K. Khoo [Australie] ; David J. Brooks [Danemark] ; James B. Rowe [Royaume-Uni] ; Roger A. Barker [Royaume-Uni] ; David J. Burn [Royaume-Uni] ; John T. O'Brien [Royaume-Uni]Source :
- Brain : a journal of neurology [ 1460-2156 ] ; 2015.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Brain Mapping, Cognition Disorders (etiology), Female, Gray Matter (pathology), Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Neuropsychological Tests, Parkinson Disease (complications), Parkinson Disease (pathology), Retrospective Studies, Severity of Illness Index, Statistics, Nonparametric.
- MESH :
- complications : Parkinson Disease.
- etiology : Cognition Disorders.
- pathology : Gray Matter, Parkinson Disease.
- Adult, Aged, Aged, 80 and over, Brain Mapping, Female, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Neuropsychological Tests, Retrospective Studies, Severity of Illness Index, Statistics, Nonparametric.
Abstract
Mild cognitive impairment in Parkinson's disease is associated with progression to dementia (Parkinson's disease dementia) in a majority of patients. Determining structural imaging biomarkers associated with prodromal Parkinson's disease dementia may allow for the earlier identification of those at risk, and allow for targeted disease modifying therapies. One hundred and five non-demented subjects with newly diagnosed idiopathic Parkinson's disease and 37 healthy matched controls had serial 3 T structural magnetic resonance imaging scans with clinical and neuropsychological assessments at baseline, which were repeated after 18 months. The Movement Disorder Society Task Force criteria were used to classify the Parkinson's disease subjects into Parkinson's disease with mild cognitive impairment (n = 39) and Parkinson's disease with no cognitive impairment (n = 66). Freesurfer image processing software was used to measure cortical thickness and subcortical volumes at baseline and follow-up. We compared regional percentage change of cortical thinning and subcortical atrophy over 18 months. At baseline, cases with Parkinson's disease with mild cognitive impairment demonstrated widespread cortical thinning relative to controls and atrophy of the nucleus accumbens compared to both controls and subjects with Parkinson's disease with no cognitive impairment. Regional cortical thickness at baseline was correlated with global cognition in the combined Parkinson's disease cohort. Over 18 months, patients with Parkinson's disease with mild cognitive impairment demonstrated more severe cortical thinning in frontal and temporo-parietal cortices, including hippocampal atrophy, relative to those with Parkinson's disease and no cognitive impairment and healthy controls, whereas subjects with Parkinson's disease and no cognitive impairment showed more severe frontal cortical thinning compared to healthy controls. At baseline, Parkinson's disease with no cognitive impairment converters showed bilateral temporal cortex thinning relative to the Parkinson's disease with no cognitive impairment stable subjects. Although loss of both cortical and subcortical volume occurs in non-demented Parkinson's disease, our longitudinal analyses revealed that Parkinson's disease with mild cognitive impairment shows more extensive atrophy and greater percentage of cortical thinning compared to Parkinson's disease with no cognitive impairment. In particular, an extension of cortical thinning in the temporo-parietal regions in addition to frontal atrophy could be a biomarker in therapeutic studies of mild cognitive impairment in Parkinson's disease for progression towards dementia.
DOI: 10.1093/brain/awv211
PubMed: 26173861
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Duncan</name><affiliation wicri:level="1"><nlm:affiliation>4 Medicine of the Elderly, Western General Hospital, Edinburgh, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>4 Medicine of the Elderly, Western General Hospital, Edinburgh</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>5 Brain and Mind Institute, University of Western Ontario, London, Canada 6 Department of Psychology, University of Western Ontario, London, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>5 Brain and Mind Institute, University of Western Ontario, London, Canada 6 Department of Psychology, University of Western Ontario, London</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>7 Griffith Health Institute and School of Medicine, Griffith University, Gold Coast, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>7 Griffith Health Institute and School of Medicine, Griffith University, Gold Coast</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>8 Division of Brain Sciences, Imperial College London, London, UK 9 Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University, Denmark.</nlm:affiliation><country xml:lang="fr">Danemark</country><wicri:regionArea>8 Division of Brain Sciences, Imperial College London, London, UK 9 Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University</wicri:regionArea></affiliation></author><author><name sortKey="Rowe, James B" sort="Rowe, James B" uniqKey="Rowe J" first="James B" last="Rowe">James B. Rowe</name><affiliation wicri:level="1"><nlm:affiliation>10 Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK 11 Medical Research Council, Cognition and Brain Sciences Unit, Cambridge, UK 12 Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>10 Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK 11 Medical Research Council, Cognition and Brain Sciences Unit, Cambridge, UK 12 Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge</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>13 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>13 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge</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>3 Institute of Neuroscience, Newcastle University, Newcastle, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>3 Institute of Neuroscience, Newcastle University, Newcastle</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>1 Department of Psychiatry, University of Cambridge, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>1 Department of Psychiatry, University of 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="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Brain Mapping</term><term>Cognition Disorders (etiology)</term><term>Female</term><term>Gray Matter (pathology)</term><term>Humans</term><term>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (pathology)</term><term>Retrospective Studies</term><term>Severity of Illness Index</term><term>Statistics, Nonparametric</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Gray Matter</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Brain Mapping</term><term>Female</term><term>Humans</term><term>Longitudinal Studies</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Retrospective Studies</term><term>Severity of Illness Index</term><term>Statistics, Nonparametric</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mild cognitive impairment in Parkinson's disease is associated with progression to dementia (Parkinson's disease dementia) in a majority of patients. Determining structural imaging biomarkers associated with prodromal Parkinson's disease dementia may allow for the earlier identification of those at risk, and allow for targeted disease modifying therapies. One hundred and five non-demented subjects with newly diagnosed idiopathic Parkinson's disease and 37 healthy matched controls had serial 3 T structural magnetic resonance imaging scans with clinical and neuropsychological assessments at baseline, which were repeated after 18 months. The Movement Disorder Society Task Force criteria were used to classify the Parkinson's disease subjects into Parkinson's disease with mild cognitive impairment (n = 39) and Parkinson's disease with no cognitive impairment (n = 66). Freesurfer image processing software was used to measure cortical thickness and subcortical volumes at baseline and follow-up. We compared regional percentage change of cortical thinning and subcortical atrophy over 18 months. At baseline, cases with Parkinson's disease with mild cognitive impairment demonstrated widespread cortical thinning relative to controls and atrophy of the nucleus accumbens compared to both controls and subjects with Parkinson's disease with no cognitive impairment. Regional cortical thickness at baseline was correlated with global cognition in the combined Parkinson's disease cohort. Over 18 months, patients with Parkinson's disease with mild cognitive impairment demonstrated more severe cortical thinning in frontal and temporo-parietal cortices, including hippocampal atrophy, relative to those with Parkinson's disease and no cognitive impairment and healthy controls, whereas subjects with Parkinson's disease and no cognitive impairment showed more severe frontal cortical thinning compared to healthy controls. At baseline, Parkinson's disease with no cognitive impairment converters showed bilateral temporal cortex thinning relative to the Parkinson's disease with no cognitive impairment stable subjects. Although loss of both cortical and subcortical volume occurs in non-demented Parkinson's disease, our longitudinal analyses revealed that Parkinson's disease with mild cognitive impairment shows more extensive atrophy and greater percentage of cortical thinning compared to Parkinson's disease with no cognitive impairment. In particular, an extension of cortical thinning in the temporo-parietal regions in addition to frontal atrophy could be a biomarker in therapeutic studies of mild cognitive impairment in Parkinson's disease for progression towards dementia.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26173861</PMID><DateCreated><Year>2015</Year><Month>09</Month><Day>26</Day></DateCreated><DateCompleted><Year>2015</Year><Month>12</Month><Day>28</Day></DateCompleted><DateRevised><Year>2017</Year><Month>01</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2156</ISSN><JournalIssue CitedMedium="Internet"><Volume>138</Volume><Issue>Pt 10</Issue><PubDate><Year>2015</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Baseline and longitudinal grey matter changes in newly diagnosed Parkinson's disease: ICICLE-PD study.</ArticleTitle><Pagination><MedlinePgn>2974-86</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/brain/awv211</ELocationID><Abstract><AbstractText>Mild cognitive impairment in Parkinson's disease is associated with progression to dementia (Parkinson's disease dementia) in a majority of patients. Determining structural imaging biomarkers associated with prodromal Parkinson's disease dementia may allow for the earlier identification of those at risk, and allow for targeted disease modifying therapies. One hundred and five non-demented subjects with newly diagnosed idiopathic Parkinson's disease and 37 healthy matched controls had serial 3 T structural magnetic resonance imaging scans with clinical and neuropsychological assessments at baseline, which were repeated after 18 months. The Movement Disorder Society Task Force criteria were used to classify the Parkinson's disease subjects into Parkinson's disease with mild cognitive impairment (n = 39) and Parkinson's disease with no cognitive impairment (n = 66). Freesurfer image processing software was used to measure cortical thickness and subcortical volumes at baseline and follow-up. We compared regional percentage change of cortical thinning and subcortical atrophy over 18 months. At baseline, cases with Parkinson's disease with mild cognitive impairment demonstrated widespread cortical thinning relative to controls and atrophy of the nucleus accumbens compared to both controls and subjects with Parkinson's disease with no cognitive impairment. Regional cortical thickness at baseline was correlated with global cognition in the combined Parkinson's disease cohort. Over 18 months, patients with Parkinson's disease with mild cognitive impairment demonstrated more severe cortical thinning in frontal and temporo-parietal cortices, including hippocampal atrophy, relative to those with Parkinson's disease and no cognitive impairment and healthy controls, whereas subjects with Parkinson's disease and no cognitive impairment showed more severe frontal cortical thinning compared to healthy controls. At baseline, Parkinson's disease with no cognitive impairment converters showed bilateral temporal cortex thinning relative to the Parkinson's disease with no cognitive impairment stable subjects. Although loss of both cortical and subcortical volume occurs in non-demented Parkinson's disease, our longitudinal analyses revealed that Parkinson's disease with mild cognitive impairment shows more extensive atrophy and greater percentage of cortical thinning compared to Parkinson's disease with no cognitive impairment. In particular, an extension of cortical thinning in the temporo-parietal regions in addition to frontal atrophy could be a biomarker in therapeutic studies of mild cognitive impairment in Parkinson's disease for progression towards dementia.</AbstractText><CopyrightInformation>© The Author (2015). Published by Oxford University Press on behalf of the Guarantors of Brain.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mak</LastName><ForeName>Elijah</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>1 Department of Psychiatry, University of Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Su</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>1 Department of Psychiatry, University of Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Williams</LastName><ForeName>Guy B</ForeName><Initials>GB</Initials><AffiliationInfo><Affiliation>2 Wolfson Brain Imaging Centre, University of Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Firbank</LastName><ForeName>Michael J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>3 Institute of Neuroscience, Newcastle University, Newcastle, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lawson</LastName><ForeName>Rachael A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>3 Institute of Neuroscience, Newcastle University, Newcastle, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yarnall</LastName><ForeName>Alison J</ForeName><Initials>AJ</Initials><AffiliationInfo><Affiliation>3 Institute of Neuroscience, Newcastle University, Newcastle, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Duncan</LastName><ForeName>Gordon W</ForeName><Initials>GW</Initials><AffiliationInfo><Affiliation>4 Medicine of the Elderly, Western General Hospital, Edinburgh, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Owen</LastName><ForeName>Adrian M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>5 Brain and Mind Institute, University of Western Ontario, London, Canada 6 Department of Psychology, University of Western Ontario, London, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khoo</LastName><ForeName>Tien K</ForeName><Initials>TK</Initials><AffiliationInfo><Affiliation>7 Griffith Health Institute and School of Medicine, Griffith University, Gold Coast, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brooks</LastName><ForeName>David J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>8 Division of Brain Sciences, Imperial College London, London, UK 9 Department of Clinical Medicine, Positron Emission Tomography Centre, Aarhus University, Denmark.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rowe</LastName><ForeName>James B</ForeName><Initials>JB</Initials><AffiliationInfo><Affiliation>10 Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK 11 Medical Research Council, Cognition and Brain Sciences Unit, Cambridge, UK 12 Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barker</LastName><ForeName>Roger A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>13 John van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Burn</LastName><ForeName>David J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>3 Institute of Neuroscience, Newcastle University, Newcastle, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>O'Brien</LastName><ForeName>John T</ForeName><Initials>JT</Initials><AffiliationInfo><Affiliation>1 Department of Psychiatry, University of 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>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>093875</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>G-1507</GrantID><Agency>Parkinson's UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>103838</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate 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