Amyloid imaging of Lewy body-associated disorders

Authors

  • Erin R. Foster OTD,

    Corresponding author
    1. Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
    2. Department of Psychiatry, Washington University School of Medicine, St Louis, MO, USA
    3. Program in Occupational Therapy, Washington University School of Medicine, St Louis, MO, USA
    • 660 South Euclid Avenue, Campus Box 8111, St. Louis, MO, USA 63110

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  • Meghan C. Campbell PhD,

    1. Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
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  • Michelle A. Burack MD, PhD,

    1. Department of Neurology, University of Rochester School of Medicine and Dentistry, St Louis, MO, USA
    2. Department of Pediatrics, University of Rochester School of Medicine and Dentistry, St Louis, MO, USA
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  • Johanna Hartlein MSN,

    1. Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
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  • Hubert P. Flores MS,

    1. Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
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  • Nigel J. Cairns PhD,

    1. Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
    2. Pathology and Immunology, Washington University School of Medicine, St Louis, MO, USA
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  • Tamara Hershey PhD,

    1. Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
    2. Department of Psychiatry, Washington University School of Medicine, St Louis, MO, USA
    3. Department of Radiology, Washington University School of Medicine, St Louis, MO, USA
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  • Joel S. Perlmutter MD

    1. Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
    2. Program in Occupational Therapy, Washington University School of Medicine, St Louis, MO, USA
    3. Department of Radiology, Washington University School of Medicine, St Louis, MO, USA
    4. Department of Anatomy and Neurobiology, Washington University School of Medicine, St Louis, MO, USA
    5. Program in Physical Therapy, Washington University School of Medicine, St Louis, MO, USA
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  • Potential conflict of interest: All authors report no financial conflicts of interest related to this research.

Abstract

Clinicopathologic studies of Parkinson disease dementia (PDD) and dementia with Lewy bodies (DLB) commonly reveal abnormal β-amyloid deposition in addition to diffuse Lewy bodies (α-synuclein aggregates), but the relationship among these neuropathologic features and the development of dementia in these disorders remains uncertain. The purpose of this study was to determine whether amyloid-β deposition detected by PET imaging with Pittsburgh Compound B (PIB) distinguishes clinical subtypes of Lewy body-associated disorders. Nine healthy controls, 8 PD with no cognitive impairment, 9 PD with mild cognitive impairment, 6 DLB, and 15 PDD patients underwent [11C]-PIB positron emission tomography imaging, clinical examination, and cognitive testing. The binding potential (BP) of PIB for predefined regions and the mean cortical BP (MCBP) were calculated for each participant. Annual longitudinal follow-up and postmortem examinations were performed on a subset of participants. Regional PIB BPs and the proportion of individuals with abnormally elevated MCBP were not significantly different across participant groups. Elevated PIB binding was associated with worse global cognitive impairment in participants with Lewy body disorders but was not associated with any other clinical or neuropsychological features, including earlier onset or faster rate of progression of cognitive impairment. These results suggest that the presence of fibrillar amyloid-β does not distinguish between clinical subtypes of Lewy body-associated disorders, although larger numbers are needed to more definitively rule out this association. Amyloid-β may modify the severity of global cognitive impairment in individuals with Lewy body-associated dementia. © 2010 Movement Disorder Society

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