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.
β-amyloid in lewy body disease is related to Alzheimer's disease-like atrophy
Article first published online: 5 DEC 2012
Copyright © 2012 Movement Disorders Society
Volume 28, Issue 2, pages 169–175, February 2013
How to Cite
Shimada, H., Shinotoh, H., Hirano, S., Miyoshi, M., Sato, K., Tanaka, N., Ota, T., Fukushi, K., Irie, T., Ito, H., Higuchi, M., Kuwabara, S. and Suhara, T. (2013), β-amyloid in lewy body disease is related to Alzheimer's disease-like atrophy. Mov. Disord., 28: 169–175. doi: 10.1002/mds.25286
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.
- Issue published online: 23 FEB 2013
- Article first published online: 5 DEC 2012
- Manuscript Accepted: 21 OCT 2012
- Manuscript Revised: 8 OCT 2012
- Manuscript Received: 30 JUN 2012
- voxel-based morphometry;
- dementia with Lewy bodies;
- Parkinson's disease with dementia;
- Alzheimer's disease;
- amyloid PET
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