| Amyloid load in Parkinson's disease dementia and Lewy body dementia measured with [11C]PIB positron emission tomography. | |
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MedLine Citation:
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PMID: 18653550 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Neuropathological studies have reported varying amounts of amyloid pathology in dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD). [11C]PIB positron emission tomography (PET) is a marker of brain amyloid deposition. The aim of this study was to quantify in vivo amyloid load in DLB and PDD compared with control subjects and subjects with Parkinson's disease (PD) without dementia. METHODS: 13 DLB, 12 PDD, 10 PD subjects and 41 age matched controls (55-82 years) were recruited. Each subject underwent clinical evaluation, neuropsychological assessment, T1 and T2 MRI, and [11C]PIB PET. The amyloid load was estimated from 60-90' target region:cerebellar [11C]PIB uptake ratios. Object maps were created by segmenting individual MRIs and convolving them with a probabilistic atlas. Cortical [11C]PIB uptake was assessed by region of interest analysis. RESULTS: The DLB cohort showed a significant increase in mean brain [11C]PIB uptake and individually 11 of the 13 subjects with DLB had a significantly increased amyloid load. In contrast, mean [11C]PIB uptake was normal for the PDD group although two of 12 patients with PDD individually showed a raised amyloid load. Where significant increases in [11C]PIB uptake were found, it was increased in cortical association areas, cingulate and striatum. None of the subjects with PD showed significantly raised cortical [11C]PIB uptake. CONCLUSION: This study suggests that amyloid load is significantly raised in over 80% of subjects with DLB, while amyloid pathology is infrequent in PDD. These in vivo PET findings suggest that the presence of amyloid in DLB could contribute to the rapid progression of dementia in this condition and that anti-amyloid strategies may be relevant. |
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Authors:
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P Edison; C C Rowe; J O Rinne; S Ng; I Ahmed; N Kemppainen; V L Villemagne; G O'Keefe; K Någren; K R Chaudhury; C L Masters; D J Brooks |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-07-24 |
Journal Detail:
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Title: Journal of neurology, neurosurgery, and psychiatry Volume: 79 ISSN: 1468-330X ISO Abbreviation: J. Neurol. Neurosurg. Psychiatr. Publication Date: 2008 Dec |
Date Detail:
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Created Date: 2008-11-17 Completed Date: 2009-01-06 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985191R Medline TA: J Neurol Neurosurg Psychiatry Country: England |
Other Details:
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Languages: eng Pagination: 1331-8 Citation Subset: IM |
Affiliation:
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Imperial College London, MRC Cyclotron Building, Hammersmith Hospital, Du Cane Road, London W120NN, UK. paul.edison@imperial.ac.uk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aged Aged, 80 and over Amyloid / metabolism, physiology* Carbon Radioisotopes / pharmacology Case-Control Studies Cohort Studies Female Humans Lewy Body Disease / diagnosis, genetics* Magnetic Resonance Imaging / methods Male Middle Aged Neuropsychology / methods Parkinson Disease / diagnosis, genetics* Positron-Emission Tomography / methods |
| Grant Support | |
ID/Acronym/Agency:
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//Medical Research Council |
| Chemical | |
Reg. No./Substance:
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0/Amyloid; 0/Carbon Radioisotopes |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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