Imaging amyloid in Parkinson's disease dementia and dementia with Lewy bodies with positron emission tomography.
Identifieur interne : 002867 ( Ncbi/Merge ); précédent : 002866; suivant : 002868Imaging amyloid in Parkinson's disease dementia and dementia with Lewy bodies with positron emission tomography.
Auteurs : David J. Brooks [Royaume-Uni]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2009.
English descriptors
- KwdEn :
- Amyloid (metabolism), Animals, Brain (pathology), Dementia (etiology), Dementia (metabolism), Dementia (pathology), Dementia (radionuclide imaging), Humans, Lewy Body Disease (metabolism), Lewy Body Disease (pathology), Lewy Body Disease (radionuclide imaging), Parkinson Disease (complications), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease (radionuclide imaging), Positron-Emission Tomography (methods).
- 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.
DOI: 10.1002/mds.22581
PubMed: 19877240
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pubmed:19877240Le document en format XML
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Brooks</name><affiliation wicri:level="3"><nlm:affiliation>MRC Clinical Sciences Centre and Division of Neuroscience, Imperial College, London, United Kingdom. david.brooks@csc.mrc.ac.uk</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Clinical Sciences Centre and Division of Neuroscience, Imperial College, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></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="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><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>Humans</term><term>Lewy Body Disease (metabolism)</term><term>Lewy Body Disease (pathology)</term><term>Lewy Body Disease (radionuclide imaging)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (radionuclide imaging)</term><term>Positron-Emission Tomography (methods)</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></textClass></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. 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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. 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