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

• Published in: Movement disorders 2013-02, Vol.28 (2), p.169-175
• Main Authors: Shimada, Hitoshi, Shinotoh, Hitoshi, Hirano, Shigeki, Miyoshi, Michie, Sato, Koichi, Tanaka, Noriko, Ota, Tsuneyoshi, Fukushi, Kiyoshi, Irie, Toshiaki, Ito, Hiroshi, Higuchi, Makoto, Kuwabara, Satoshi, Suhara, Tetsuya
• Format: Article
• Language: English
• Subjects: Aged; Aging - physiology; Alzheimer Disease - diagnostic imaging; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Alzheimer's disease; Amyloid beta-Peptides - analysis; Amyloid beta-Peptides - metabolism; amyloid PET; Analysis of Variance; Atrophy; Benzothiazoles; Dementia - metabolism; Dementia - pathology; Dementia - psychology; dementia with Lewy bodies; Female; Humans; Image Processing, Computer-Assisted; Lewy Body Disease - diagnostic imaging; Lewy Body Disease - metabolism; Lewy Body Disease - pathology; Magnetic Resonance Imaging; Male; Middle Aged; Neuropsychological Tests; Parkinson Disease - metabolism; Parkinson Disease - pathology; Parkinson Disease - psychology; Parkinson's disease with dementia; Positron-Emission Tomography; Radiopharmaceuticals; voxel-based morphometry
• ISSN: 0885-3185; 1531-8257
• DOI: 10.1002/mds.25286

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