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β-amyloid in lewy body disease is related to Alzheimer's disease-like atrophy

Authors

  • Hitoshi Shimada MD, PhD,

    1. Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba, Japan
    2. Section for Human Neurophysiology, Research Center for Frontier Medical Engineering, Chiba University, Chiba, Japan
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  • Hitoshi Shinotoh MD, PhD,

    1. Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba, Japan
    2. Neurology Chiba, Chiba, Japan
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  • Shigeki Hirano MD, PhD,

    1. Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba, Japan
    2. Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan
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  • Michie Miyoshi MD, PhD,

    1. Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba, Japan
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  • Koichi Sato MD, PhD,

    1. Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba, Japan
    2. Department of Psychiatry, Teikyo University Chiba Medical Center, Chiba, Japan
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  • Noriko Tanaka MD, PhD,

    1. Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba, Japan
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  • Tsuneyoshi Ota MD, PhD,

    1. Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba, Japan
    2. Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan
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  • Kiyoshi Fukushi PhD,

    1. Molecular Imaging Center, Molecular Probe Program, National Institute of Radiological Sciences, Chiba, Japan
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  • Toshiaki Irie PhD,

    1. Molecular Imaging Center, Molecular Probe Program, National Institute of Radiological Sciences, Chiba, Japan
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  • Hiroshi Ito MD, PhD,

    1. Molecular Imaging Center, Biophysics Program, National Institute of Radiological Sciences, Chiba, Japan
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  • Makoto Higuchi MD, PhD,

    1. Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba, Japan
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  • Satoshi Kuwabara MD, PhD,

    1. Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan
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  • Tetsuya Suhara MD, PhD

    Corresponding author
    1. Molecular Imaging Center, Molecular Neuroimaging Program, National Institute of Radiological Sciences, Chiba, Japan
    • Correspondence to: Dr. Tetsuya Suhara, Molecular Neuroimaging Program, Molecular Imaging Center, National Institute of Radiological Sciences, 4-9-1 Anagawa, Inage-ku, Chiba-shi, Chiba, 263-8555, Japan; suhara@nirs.go.jp

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  • Funding agencies: A part of this work was supported by the Japan Advanced Molecular Imaging Program of the Ministry of Education, Culture, Sports, Science, and Technology, Japan, a Grant-in-Aid for Scientific Research on Innovative Areas from the Ministry of Education, Culture, Sports, Science, and Technology, Japan, and a Grant-in-Aid for Comprehensive Research on Dementia (no. 11103404) from the Ministry of Health, Labor, and Welfare.

  • Relevant conflicts of interest/financial disclosures: Nothing to report.

  • Full financial disclosures and author roles may be found in the online version of this article.

Abstract

The aim of this study was to investigate whether amyloid deposition is associated with Alzheimer's disease (AD)-like cortical atrophy in Lewy body (LB) disease (LBD). Participants included 15 LBD with dementia patients (8 with dementia with Lewy bodies [DLB] and 7 with Parkinson's disease [PD] with dementia [PDD]), 13 AD patients, and 17 healthy controls. Age, gender, and Mini–Mental State Examination scores were matched between patient groups. All subjects underwent PET scans with [11C]Pittsburgh Compound B to measure brain amyloid deposition as well as three-dimensional T1-weighted MRI. Gray-matter volumes (GMVs) were estimated by voxel-based morphometry. Volumes-of-interest analyses were also performed. Forty percent of the 15 DLB/PDD patients were amyloid positive, whereas all AD patients and none of the healthy controls were amyloid positive. Amyloid-positive DLB/PDD and AD patients showed very similar patterns of cortical atrophy in the parahippocampal area and lateral temporal and parietal cortices, with 95.2% of cortical atrophy distribution being overlapped. In contrast, amyloid-negative DLB/PDD patients had no significant cortical atrophy. Compared to healthy controls, parahippocampal GMVs were reduced by 26% in both the amyloid-positive DLB/PDD and AD groups and by 10% in the amyloid-negative DLB/PDD group. The results suggest that amyloid deposition is associated with AD-like atrophy in DLB/PDD patients. Early intervention against amyloid may prevent or delay AD-like atrophy in DLB/PDD patients with amyloid deposition. © 2012 Movement Disorder Society

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