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Amyloid load in Parkinson’s disease dementia and Lewy Body dementia measured with [11C]PIB-PET
  1. Paul Edison (paul.edison{at}imperial.ac.uk)
  1. MRC clinical science centre, Imperial College London, United Kingdom
    1. Christopher C Rowe (christopher.rowe{at}austin.org.au)
    1. Austin Hospital, University of Melbourne, Australia
      1. Juha O Rinne (juha.rinne{at}fimnet.fi)
      1. Turku PET Centre, University of Turku, Finland
        1. Steven Ng
        1. Centre for PET, Austin Health, Melbourne and Colin L Masters - Dept. Pathology, Melbourne, Australia
          1. Imtiaz Ahmed (imtiaz.ahmed{at}imperial.ac.uk)
          1. MRC Clinical Sciences Centre and Division of Neuroscience, Imperial College London, United Kingdom
            1. Nina Kemppainen (juha.rinne{at}fimnet.fi)
            1. Turku PET Centre, University of Turku, Finland
              1. Victor L Villemagne (christopher.rowe{at}austin.org.au)
              1. Centre for PET, Austin Health, Melbourne and Colin L Masters - Dept. Pathology, Melbourne, Australia
                1. Graeme O'Keefe (christopher.rowe{at}austin.org.au)
                1. Centre for PET, Austin Health, Melbourne and Colin L Masters - Dept. Pathology, Melbourne, Australia
                  1. Kjell Någren (juha.rinne{at}fimnet.fi)
                  1. Turku PET Centre, University of Turku, Finland
                    1. Ray Chaudhuri (ray.chaudhuri{at}uhl.nhs.uk)
                    1. Kings College London, United Kingdom
                      1. Colin L Masters (christopher.rowe{at}austin.org.au)
                      1. Austin Hospital, University of Melbourne, Australia
                        1. D J Brooks (david.brooks{at}csc.mrc.ac.uk)
                        1. MRC Clinical Sciences Centre and Division of Neuroscience, Imperial College London, United Kingdom

                          Abstract

                          Background: Neuropathological studies have reported varying amounts of amyloid pathology in dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). [11C]PIB-PET is a marker of brain amyloid deposition. The aim of our study was to quantify in vivo amyloid load in DLB and PDD and to compare this with that in control subjects and Parkinson’s disease subjects without dementia (PD).

                          Methods: 13 DLB, 12 PDD, 10 PD subjects, and 41 age-matched controls (55-82 yrs) 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 eleven of the 13 DLB subjects had a significantly increased amyloid load. In contrast, mean [11C]PIB-uptake was normal for the PDD group though 2 of 12 PDD patients 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 PD subjects showed significantly raised cortical [11C]PIB-uptake.

                          Conclusion: This study suggests that amyloid load is significantly raised in over 80% of DLB subjects, 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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