title: Pathological entity of dementia with Lewy bodies and its differentiation from Alzheimer's disease.
abstract: We reclassified the pathological subtypes of dementia with Lewy bodies (DLB), based on both Lewy pathology and Alzheimer pathology, to clarify the pathological entity of DLB and the boundary between DLB and Alzheimer's disease (AD) in autopsied cases, using both pathological and immunohistochemical methods. DLB was classified as either limbic type or neocortical type according to the degree of Lewy pathology including Lewy bodies (LB) and LB-related neurites by our staging, and was classified as pure form, common form or AD form according to the degree of Alzheimer pathology including neurofibrillary tangles (NFT) and amyloid deposits by Braak staging. These combined subtypes were lined up on a spectrum, not only with Lewy pathology but also with other DLB-related pathologies including Alzheimer pathology, neuronal loss in the substantia nigra, spongiform change in the transentorhinal cortex and LB-related neurites in the CA2-3 region. In contrast, the Lewy pathology of AD did not meet the stages of Lewy pathology in DLB, and there were scarcely any similarities in other DLB-related pathologies between AD and DLB. In addition, the Lewy pathology of AD had characteristics different from that of DLB, including the coexistence rate of LB with NFT, and the immunohistochemical and immunoelectron microscopic findings of LB and LB-related neurites. These findings suggest that DLB is a distinctive pathological entity that can be differentiated from AD, although it shows some pathological subtypes.
authors.affiliation: Department of Psychiatry, Yokohama City University School of Medicine, 3-9 Fukuura, Kanazawa-ku, 236-0004, Yokohama, Japan.
authors.forename: Wami
authors.initials: W
authors.lastname: Marui
authors.forename: Eizo
authors.initials: E
authors.lastname: Iseki
authors.forename: Masanori
authors.initials: M
authors.lastname: Kato
authors.forename: Hiroyasu
authors.initials: H
authors.lastname: Akatsu
authors.forename: Kenji
authors.initials: K
authors.lastname: Kosaka
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology*; D000682:Amyloid / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000473:pathology; D004268:DNA-Binding Proteins / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D016631:Lewy Bodies / Q000473:pathology*; D020961:Lewy Body Disease / Q000145:classification* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism; D016874:Neurofibrillary Tangles / Q000473:pathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D063146:Polycomb-Group Proteins; D011180:Postmortem Changes; D051843:Synucleins; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D000682:Amyloid; D016229:Amyloid beta-Peptides; D004268:DNA-Binding Proteins; D009419:Nerve Tissue Proteins; C112309:PHF1 protein, human; D063146:Polycomb-Group Proteins; D051843:Synucleins; D014157:Transcription Factors