Imaging amyloid in Parkinson's disease dementia and dementia with Lewy bodies with positron emission tomography
Identifieur interne : 002262 ( Main/Exploration ); précédent : 002261; suivant : 002263Imaging amyloid in Parkinson's disease dementia and dementia with Lewy bodies with positron emission tomography
Auteurs : David J. Brooks [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2009.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Amyloid, Amyloid (metabolism), Animals, Brain (pathology), Dementia (etiology), Dementia (metabolism), Dementia (pathology), Dementia (radionuclide imaging), Emission tomography, Humans, Lewy Body Disease (metabolism), Lewy Body Disease (pathology), Lewy Body Disease (radionuclide imaging), Lewy body, Lewy body dementia, Nervous system diseases, PET, PIB, Parkinson, Parkinson Disease (complications), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease (radionuclide imaging), Parkinson disease, Positron emission tomography, Positron-Emission Tomography (methods), amyloid, dementia.
- MESH :
- chemical , metabolism : Amyloid.
- complications : Parkinson Disease.
- etiology : Dementia.
- metabolism : Dementia, Lewy Body Disease, Parkinson Disease.
- methods : Positron-Emission Tomography.
- pathology : Brain, Dementia, Lewy Body Disease, Parkinson Disease.
- radionuclide imaging : Dementia, Lewy Body Disease, Parkinson Disease.
- Animals, Humans.
Abstract
Although Parkinson's disease with later dementia (PDD) and dementia with Lewy bodies (DLB) are pathologically characterized by the presence of intraneuronal Lewy inclusion bodies, amyloid deposition is also associated to varying degrees with both these disorders. Fibrillar amyloid load can now be quantitated in vivo with positron emission tomography (PET) using imaging biomarkers. Here the reported findings of 11C‐PIB PET studies concerning the amyloid load associated with PD and its influence on dementia are reviewed. It is concluded that the presence of amyloid acts to accelerate the dementia process in Lewy body disorders, though has little influence on its nature. Anti‐amyloid strategies could be a relevant approach for slowing dementia in a number of DLB and PDD cases. © 2009 Movement Disorder Society
Url:
DOI: 10.1002/mds.22581
Affiliations:
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Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009">2009</date><biblScope unit="vol">24</biblScope><biblScope unit="issue">S2</biblScope><biblScope unit="page" from="S742">S742</biblScope><biblScope unit="page" to="S747">S747</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">8065BB837B02C11FEB0F383F60B9C6785B037CE0</idno><idno type="DOI">10.1002/mds.22581</idno><idno type="ArticleID">MDS22581</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amyloid</term><term>Amyloid (metabolism)</term><term>Animals</term><term>Brain (pathology)</term><term>Dementia (etiology)</term><term>Dementia (metabolism)</term><term>Dementia (pathology)</term><term>Dementia (radionuclide imaging)</term><term>Emission tomography</term><term>Humans</term><term>Lewy Body Disease (metabolism)</term><term>Lewy Body Disease (pathology)</term><term>Lewy Body Disease (radionuclide imaging)</term><term>Lewy body</term><term>Lewy body dementia</term><term>Nervous system diseases</term><term>PET</term><term>PIB</term><term>Parkinson</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (radionuclide imaging)</term><term>Parkinson disease</term><term>Positron emission tomography</term><term>Positron-Emission Tomography (methods)</term><term>amyloid</term><term>dementia</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amyloid</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dementia</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dementia</term><term>Lewy Body Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Positron-Emission Tomography</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Dementia</term><term>Lewy Body Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Dementia</term><term>Lewy Body Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Amyloïde</term><term>Corps Lewy</term><term>Démence à corps de Lewy</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Tomographie par émission de positons</term><term>Tomoscintigraphie</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although Parkinson's disease with later dementia (PDD) and dementia with Lewy bodies (DLB) are pathologically characterized by the presence of intraneuronal Lewy inclusion bodies, amyloid deposition is also associated to varying degrees with both these disorders. Fibrillar amyloid load can now be quantitated in vivo with positron emission tomography (PET) using imaging biomarkers. Here the reported findings of 11C‐PIB PET studies concerning the amyloid load associated with PD and its influence on dementia are reviewed. It is concluded that the presence of amyloid acts to accelerate the dementia process in Lewy body disorders, though has little influence on its nature. Anti‐amyloid strategies could be a relevant approach for slowing dementia in a number of DLB and PDD cases. © 2009 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. 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