Imaging amyloid in Parkinson's disease dementia and dementia with Lewy bodies with positron emission tomography
Identifieur interne : 002480 ( Main/Corpus ); précédent : 002479; suivant : 002481Imaging amyloid in Parkinson's disease dementia and dementia with Lewy bodies with positron emission tomography
Auteurs : David J. BrooksSource :
- Movement Disorders [ 0885-3185 ] ; 2009.
English descriptors
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
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DOI: 10.1002/mds.22581
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ISTEX:8065BB837B02C11FEB0F383F60B9C6785B037CE0Le document en format XML
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Fibrillar amyloid load can now be quantitated in vivo with positron emission tomography (PET) using imaging biomarkers. Here the reported findings of <sup>11</sup>C‐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</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflicts of interest: David Brooks is the sole author of this work. He holds a part‐time position as Head of Neurology with Medical Diagnostics, GE Healthcare, who owns the commercial rights to PIB but did not resource any of the studies quoted.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Imaging amyloid in Parkinson's disease dementia and dementia with Lewy bodies with positron emission tomography</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Amyloid in Parkinson's Disease Dementia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Imaging amyloid in Parkinson's disease dementia and dementia with Lewy bodies with positron emission tomography</title></titleInfo><name type="personal"><namePart type="given">David J.</namePart><namePart type="family">Brooks</namePart><namePart type="termsOfAddress">MD, DSc, FRCP, FMedSci</namePart><affiliation>MRC Clinical Sciences Centre and Division of Neuroscience, Imperial College, London, United Kingdom</affiliation><description>Correspondence: Cyclotron Building, Hammersmith Hospital, Du Cane Road, London, W12 0NN, United Kingdom</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009</dateIssued><dateCaptured encoding="w3cdtf">2008-12-08</dateCaptured><dateValid encoding="w3cdtf">2009-03-06</dateValid><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">1</extent><extent unit="references">38</extent><extent unit="words">4448</extent></physicalDescription><abstract 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</abstract><note type="content">*Potential conflicts of interest: David Brooks is the sole author of this work. He holds a part‐time position as Head of Neurology with Medical Diagnostics, GE Healthcare, who owns the commercial rights to PIB but did not resource any of the studies quoted.</note><subject lang="en"><genre>Keywords</genre><topic>PET</topic><topic>amyloid</topic><topic>dementia</topic><topic>Parkinson</topic><topic>Lewy body</topic><topic>PIB</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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