β-Amyloid in Lewy body disease is related to Alzheimer's disease-like atrophy.
Identifieur interne : 000694 ( Main/Exploration ); précédent : 000693; suivant : 000695β-Amyloid in Lewy body disease is related to Alzheimer's disease-like atrophy.
Auteurs : Hitoshi Shimada [Japon] ; Hitoshi Shinotoh ; Shigeki Hirano ; Michie Miyoshi ; Koichi Sato ; Noriko Tanaka ; Tsuneyoshi Ota ; Kiyoshi Fukushi ; Toshiaki Irie ; Hiroshi Ito ; Makoto Higuchi ; Satoshi Kuwabara ; Tetsuya SuharaSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Aged, Aging (physiology), Alzheimer Disease (metabolism), Alzheimer Disease (pathology), Alzheimer Disease (radionuclide imaging), Amyloid beta-Peptides (analysis), Amyloid beta-Peptides (metabolism), Analysis of Variance, Atrophy, Benzothiazoles (diagnostic use), Dementia (metabolism), Dementia (pathology), Dementia (psychology), Female, Humans, Image Processing, Computer-Assisted, Lewy Body Disease (metabolism), Lewy Body Disease (pathology), Lewy Body Disease (radionuclide imaging), Magnetic Resonance Imaging, Male, Middle Aged, Neuropsychological Tests, Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease (psychology), Positron-Emission Tomography, Radiopharmaceuticals.
- MESH :
- chemical , analysis : Amyloid beta-Peptides.
- chemical , diagnostic use : Benzothiazoles.
- metabolism : Alzheimer Disease, Amyloid beta-Peptides, Dementia, Lewy Body Disease, Parkinson Disease.
- pathology : Alzheimer Disease, Dementia, Lewy Body Disease, Parkinson Disease.
- physiology : Aging.
- psychology : Dementia, Parkinson Disease.
- radionuclide imaging : Alzheimer Disease, Lewy Body Disease.
- Aged, Analysis of Variance, Atrophy, Female, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Middle Aged, Neuropsychological Tests, Positron-Emission Tomography, Radiopharmaceuticals.
Abstract
The aim of this study was to investigate whether amyloid deposition is associated with Alzheimer's disease (AD)-like cortical atrophy in Lewy body (LB) disease (LBD). Participants included 15 LBD with dementia patients (8 with dementia with Lewy bodies [DLB] and 7 with Parkinson's disease [PD] with dementia [PDD]), 13 AD patients, and 17 healthy controls. Age, gender, and Mini-Mental State Examination scores were matched between patient groups. All subjects underwent PET scans with [(11)C]Pittsburgh Compound B to measure brain amyloid deposition as well as three-dimensional T1-weighted MRI. Gray-matter volumes (GMVs) were estimated by voxel-based morphometry. Volumes-of-interest analyses were also performed. Forty percent of the 15 DLB/PDD patients were amyloid positive, whereas all AD patients and none of the healthy controls were amyloid positive. Amyloid-positive DLB/PDD and AD patients showed very similar patterns of cortical atrophy in the parahippocampal area and lateral temporal and parietal cortices, with 95.2% of cortical atrophy distribution being overlapped. In contrast, amyloid-negative DLB/PDD patients had no significant cortical atrophy. Compared to healthy controls, parahippocampal GMVs were reduced by 26% in both the amyloid-positive DLB/PDD and AD groups and by 10% in the amyloid-negative DLB/PDD group. The results suggest that amyloid deposition is associated with AD-like atrophy in DLB/PDD patients. Early intervention against amyloid may prevent or delay AD-like atrophy in DLB/PDD patients with amyloid deposition.
DOI: 10.1002/mds.25286
PubMed: 23225334
Affiliations:
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Le document en format XML
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Hirano</name></author><author><name sortKey="Miyoshi, Michie" sort="Miyoshi, Michie" uniqKey="Miyoshi M" first="Michie" last="Miyoshi">Michie Miyoshi</name></author><author><name sortKey="Sato, Koichi" sort="Sato, Koichi" uniqKey="Sato K" first="Koichi" last="Sato">Koichi Sato</name></author><author><name sortKey="Tanaka, Noriko" sort="Tanaka, Noriko" uniqKey="Tanaka N" first="Noriko" last="Tanaka">Noriko Tanaka</name></author><author><name sortKey="Ota, Tsuneyoshi" sort="Ota, Tsuneyoshi" uniqKey="Ota T" first="Tsuneyoshi" last="Ota">Tsuneyoshi Ota</name></author><author><name sortKey="Fukushi, Kiyoshi" sort="Fukushi, Kiyoshi" uniqKey="Fukushi K" first="Kiyoshi" last="Fukushi">Kiyoshi Fukushi</name></author><author><name sortKey="Irie, Toshiaki" sort="Irie, Toshiaki" uniqKey="Irie T" first="Toshiaki" last="Irie">Toshiaki Irie</name></author><author><name sortKey="Ito, Hiroshi" sort="Ito, Hiroshi" uniqKey="Ito H" first="Hiroshi" last="Ito">Hiroshi Ito</name></author><author><name sortKey="Higuchi, Makoto" sort="Higuchi, Makoto" uniqKey="Higuchi M" first="Makoto" last="Higuchi">Makoto Higuchi</name></author><author><name sortKey="Kuwabara, Satoshi" sort="Kuwabara, Satoshi" uniqKey="Kuwabara S" first="Satoshi" last="Kuwabara">Satoshi Kuwabara</name></author><author><name sortKey="Suhara, Tetsuya" sort="Suhara, Tetsuya" uniqKey="Suhara T" first="Tetsuya" last="Suhara">Tetsuya Suhara</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="doi">10.1002/mds.25286</idno><idno type="RBID">pubmed:23225334</idno><idno type="pmid">23225334</idno><idno type="wicri:Area/PubMed/Corpus">000B40</idno><idno type="wicri:Area/PubMed/Curation">000B40</idno><idno type="wicri:Area/PubMed/Checkpoint">000714</idno><idno type="wicri:Area/Ncbi/Merge">003923</idno><idno type="wicri:Area/Ncbi/Curation">003923</idno><idno type="wicri:Area/Ncbi/Checkpoint">003923</idno><idno type="wicri:Area/Main/Merge">000694</idno><idno type="wicri:Area/Main/Curation">000694</idno><idno type="wicri:Area/Main/Exploration">000694</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">β-Amyloid in Lewy body disease is related to Alzheimer's disease-like atrophy.</title><author><name sortKey="Shimada, Hitoshi" sort="Shimada, Hitoshi" uniqKey="Shimada H" first="Hitoshi" last="Shimada">Hitoshi Shimada</name><affiliation wicri:level="1"><nlm:affiliation>Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba</wicri:regionArea><wicri:noRegion>Chiba</wicri:noRegion></affiliation></author><author><name sortKey="Shinotoh, Hitoshi" sort="Shinotoh, Hitoshi" uniqKey="Shinotoh H" first="Hitoshi" last="Shinotoh">Hitoshi Shinotoh</name></author><author><name sortKey="Hirano, Shigeki" sort="Hirano, Shigeki" uniqKey="Hirano S" first="Shigeki" last="Hirano">Shigeki Hirano</name></author><author><name sortKey="Miyoshi, Michie" sort="Miyoshi, Michie" uniqKey="Miyoshi M" first="Michie" last="Miyoshi">Michie Miyoshi</name></author><author><name sortKey="Sato, Koichi" sort="Sato, Koichi" uniqKey="Sato K" first="Koichi" last="Sato">Koichi Sato</name></author><author><name sortKey="Tanaka, Noriko" sort="Tanaka, Noriko" uniqKey="Tanaka N" first="Noriko" last="Tanaka">Noriko Tanaka</name></author><author><name sortKey="Ota, Tsuneyoshi" sort="Ota, Tsuneyoshi" uniqKey="Ota T" first="Tsuneyoshi" last="Ota">Tsuneyoshi Ota</name></author><author><name sortKey="Fukushi, Kiyoshi" sort="Fukushi, Kiyoshi" uniqKey="Fukushi K" first="Kiyoshi" last="Fukushi">Kiyoshi Fukushi</name></author><author><name sortKey="Irie, Toshiaki" sort="Irie, Toshiaki" uniqKey="Irie T" first="Toshiaki" last="Irie">Toshiaki Irie</name></author><author><name sortKey="Ito, Hiroshi" sort="Ito, Hiroshi" uniqKey="Ito H" first="Hiroshi" last="Ito">Hiroshi Ito</name></author><author><name sortKey="Higuchi, Makoto" sort="Higuchi, Makoto" uniqKey="Higuchi M" first="Makoto" last="Higuchi">Makoto Higuchi</name></author><author><name sortKey="Kuwabara, Satoshi" sort="Kuwabara, Satoshi" uniqKey="Kuwabara S" first="Satoshi" last="Kuwabara">Satoshi Kuwabara</name></author><author><name sortKey="Suhara, Tetsuya" sort="Suhara, Tetsuya" uniqKey="Suhara T" first="Tetsuya" last="Suhara">Tetsuya Suhara</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aging (physiology)</term><term>Alzheimer Disease (metabolism)</term><term>Alzheimer Disease (pathology)</term><term>Alzheimer Disease (radionuclide imaging)</term><term>Amyloid beta-Peptides (analysis)</term><term>Amyloid beta-Peptides (metabolism)</term><term>Analysis of Variance</term><term>Atrophy</term><term>Benzothiazoles (diagnostic use)</term><term>Dementia (metabolism)</term><term>Dementia (pathology)</term><term>Dementia (psychology)</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Lewy Body Disease (metabolism)</term><term>Lewy Body Disease (pathology)</term><term>Lewy Body Disease (radionuclide imaging)</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (psychology)</term><term>Positron-Emission Tomography</term><term>Radiopharmaceuticals</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Amyloid beta-Peptides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Benzothiazoles</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Alzheimer Disease</term><term>Amyloid beta-Peptides</term><term>Dementia</term><term>Lewy Body Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Dementia</term><term>Lewy Body Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Aging</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Alzheimer Disease</term><term>Lewy Body Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Atrophy</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Positron-Emission Tomography</term><term>Radiopharmaceuticals</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The aim of this study was to investigate whether amyloid deposition is associated with Alzheimer's disease (AD)-like cortical atrophy in Lewy body (LB) disease (LBD). Participants included 15 LBD with dementia patients (8 with dementia with Lewy bodies [DLB] and 7 with Parkinson's disease [PD] with dementia [PDD]), 13 AD patients, and 17 healthy controls. Age, gender, and Mini-Mental State Examination scores were matched between patient groups. All subjects underwent PET scans with [(11)C]Pittsburgh Compound B to measure brain amyloid deposition as well as three-dimensional T1-weighted MRI. Gray-matter volumes (GMVs) were estimated by voxel-based morphometry. Volumes-of-interest analyses were also performed. Forty percent of the 15 DLB/PDD patients were amyloid positive, whereas all AD patients and none of the healthy controls were amyloid positive. Amyloid-positive DLB/PDD and AD patients showed very similar patterns of cortical atrophy in the parahippocampal area and lateral temporal and parietal cortices, with 95.2% of cortical atrophy distribution being overlapped. In contrast, amyloid-negative DLB/PDD patients had no significant cortical atrophy. Compared to healthy controls, parahippocampal GMVs were reduced by 26% in both the amyloid-positive DLB/PDD and AD groups and by 10% in the amyloid-negative DLB/PDD group. The results suggest that amyloid deposition is associated with AD-like atrophy in DLB/PDD patients. Early intervention against amyloid may prevent or delay AD-like atrophy in DLB/PDD patients with amyloid deposition.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><noCountry><name sortKey="Fukushi, Kiyoshi" sort="Fukushi, Kiyoshi" uniqKey="Fukushi K" first="Kiyoshi" last="Fukushi">Kiyoshi Fukushi</name><name sortKey="Higuchi, Makoto" sort="Higuchi, Makoto" uniqKey="Higuchi M" first="Makoto" last="Higuchi">Makoto Higuchi</name><name sortKey="Hirano, Shigeki" sort="Hirano, Shigeki" uniqKey="Hirano S" first="Shigeki" last="Hirano">Shigeki Hirano</name><name sortKey="Irie, Toshiaki" sort="Irie, Toshiaki" uniqKey="Irie T" first="Toshiaki" last="Irie">Toshiaki Irie</name><name sortKey="Ito, Hiroshi" sort="Ito, Hiroshi" uniqKey="Ito H" first="Hiroshi" last="Ito">Hiroshi Ito</name><name sortKey="Kuwabara, Satoshi" sort="Kuwabara, Satoshi" uniqKey="Kuwabara S" first="Satoshi" last="Kuwabara">Satoshi Kuwabara</name><name sortKey="Miyoshi, Michie" sort="Miyoshi, Michie" uniqKey="Miyoshi M" first="Michie" last="Miyoshi">Michie Miyoshi</name><name sortKey="Ota, Tsuneyoshi" sort="Ota, Tsuneyoshi" uniqKey="Ota T" first="Tsuneyoshi" last="Ota">Tsuneyoshi Ota</name><name sortKey="Sato, Koichi" sort="Sato, Koichi" uniqKey="Sato K" first="Koichi" last="Sato">Koichi Sato</name><name sortKey="Shinotoh, Hitoshi" sort="Shinotoh, Hitoshi" uniqKey="Shinotoh H" first="Hitoshi" last="Shinotoh">Hitoshi Shinotoh</name><name sortKey="Suhara, Tetsuya" sort="Suhara, Tetsuya" uniqKey="Suhara T" first="Tetsuya" last="Suhara">Tetsuya Suhara</name><name sortKey="Tanaka, Noriko" sort="Tanaka, Noriko" uniqKey="Tanaka N" first="Noriko" last="Tanaka">Noriko Tanaka</name></noCountry><country name="Japon"><noRegion><name sortKey="Shimada, Hitoshi" sort="Shimada, Hitoshi" uniqKey="Shimada H" first="Hitoshi" last="Shimada">Hitoshi Shimada</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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