title: Distribution of cerebral amyloid deposition and its relevance to clinical phenotype in Lewy body dementia.
abstract: Parkinson's disease dementia (PDD) and dementia with Lewy bodies (DLB) are clinically distinguished based only on the duration of parkinsonism prior to dementia. It is known that there is considerable pathological overlap between these two conditions, but the pathological difference between them remains unknown. We evaluated Alzheimer-type pathology in 30 brains of patients with Lewy body dementia using standardized methods based on those of the Brain-Net Europe (BNE) Consortium. Only 2 of 13 PDD cases (15%) showed Aβ-immunoreactive pathology in the midbrain (amyloid phase IV). In contrast, 12 of 17 DLB cases (71%) exhibited midbrain involvement. Four of the DLB cases (24%) but none of the PDD cases exhibited Aβ-immunoreactive pathology in the cerebellum (amyloid phase V). The ratio of cases with subtentorial involvement of amyloid deposition was significantly higher in DLB than in PDD. The median of amyloid phases was significantly greater in DLB than in PDD, but there was no difference in neurofibrillary tangle (NFT) Braak stages or in Lewy body scores. When patients were classified according to whether dementia or parkinsonism had occurred first, the rate of dementia having occurred first was significantly greater in amyloid phase IV and V than in phase 0-I, with phase III in the middle, though there was no significant difference in median NFT Braak stage or mean Lewy body score associated with amyloid phase. These results suggest that amyloid deposition may contribute to the timing of the onset of dementia relative to that of parkinsonism in Lewy body dementia.
authors.affiliation: PET/CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Koto-ku, Tokyo 136-0075, Japan. fujishiro17@hotmail.co.jp
authors.forename: Hiroshige
authors.initials: H
authors.lastname: Fujishiro
authors.forename: Eizo
authors.initials: E
authors.lastname: Iseki
authors.forename: Shinji
authors.initials: S
authors.lastname: Higashi
authors.forename: Koji
authors.initials: K
authors.lastname: Kasanuki
authors.forename: Norio
authors.initials: N
authors.lastname: Murayama
authors.forename: Takashi
authors.initials: T
authors.lastname: Togo
authors.forename: Omi
authors.initials: O
authors.lastname: Katsuse
authors.forename: Hirotake
authors.initials: H
authors.lastname: Uchikado
authors.forename: Naoya
authors.initials: N
authors.lastname: Aoki
authors.forename: Kenji
authors.initials: K
authors.lastname: Kosaka
authors.forename: Heii
authors.initials: H
authors.lastname: Arai
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Sato
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D003937:Diagnosis, Differential; D005260:Female; D006801:Humans; D016631:Lewy Bodies / Q000378:metabolism; D020961:Lewy Body Disease / Q000378:metabolism* / Q000473:pathology*; D008297:Male; D016874:Neurofibrillary Tangles / Q000378:metabolism; D010300:Parkinson Disease / Q000378:metabolism* / Q000473:pathology*; D051844:alpha-Synuclein / Q000378:metabolism; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D015415:Biomarkers; D051844:alpha-Synuclein; D016875:tau Proteins