b-Amyloid in Lewy Body Disease Is Related to Alzheimer’s Disease-Like Atrophy Hitoshi Shimada, MD, PhD, 1,2 Hitoshi Shinotoh, MD, PhD, 1,3 Shigeki Hirano, MD, PhD, 1,4 Michie Miyoshi, MD, PhD, 1 Koichi Sato, MD, PhD, 1,5 Noriko Tanaka, MD, PhD, 1 Tsuneyoshi Ota, MD, PhD, 1,6 Kiyoshi Fukushi, PhD, 7 Toshiaki Irie, PhD, 7 Hiroshi Ito, MD, PhD, 8 Makoto Higuchi, MD, PhD, 1 Satoshi Kuwabara, MD, PhD, 4 and Tetsuya Suhara, MD, PhD 1 * 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 3 Neurology Chiba, Chiba, Japan 4 Department of Neurology, Graduate School of Medicine, Chiba University, Chiba, Japan 5 Department of Psychiatry, Teikyo University Chiba Medical Center, Chiba, Japan 6 Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan 7 Molecular Imaging Center, Molecular Probe Program, National Institute of Radiological Sciences, Chiba, Japan 8 Molecular Imaging Center, Biophysics Program, National Institute of Radiological Sciences, Chiba, Japan 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) dis- ease (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 [ 11 C]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, parahippo- campal GMVs were reduced by 26% in both the amyloid- positive DLB/PDD and AD groups and by 10% in the amy- loid-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. V C 2012 Movement Disorder Society Key Words: voxel-based morphometry; dementia with Lewy bodies; Parkinson’s disease with dementia; Alzheimer’s disease; amyloid PET Dementia with Lewy bodies (DLB) and Parkinson’s disease (PD) with dementia (PDD) are categorized as belonging to the same spectrum: LBD with dementia. 1 In addition to pathognomonic Lewy body (LB) pathol- ogy, DLB/PDD patients frequently have Alzheimer’s disease (AD)-type pathology, particularly amyloid beta (Ab) plaque. 2 The contribution of Ab to the develop- ment of DLB/PDD remains unclear. [ 11 C]Pittsburgh compound B (PIB) is a well-estab- lished compound for amyloid imaging with PET. 3 An in vitro binding study indicated that the PIB retention observed in DLB is largely attributable to PIB binding to Ab plaque, but not to LBs. 4 More than half of DLB patients and approximately one third of PDD patients had cortical Ab burden in previous studies using ------------------------------------------------------------ Additional Supporting Information may be found in the online version of this article. *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 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. Received: 30 June 2012; Revised: 8 October 2012; Accepted: 21 October 2012 Published online 5 December 2012 in Wiley Online Library (wileyonlinelibrary.com). DOI: 10.1002/mds.25286 RESEARCH ARTICLE Movement Disorders, Vol. 28, No. 2, 2013 169