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Deposition of  -Amyloid Subtypes 40 and 42 Differentiates Dementia With Lewy Bodies From Alzheimer Disease
Carol F. Lippa, MD;
Kazuharu Ozawa, PhD;
David M. A. Mann, PhD;
Kazuhiro Ishii, MD;
Thomas W. Smith, MD;
Shigeki Arawaka, MD;
Hiroshi Mori, PhD
Arch Neurol. 1999;56:1111-1118.
Background Alterations in the metabolism of the amyloid precursor protein and the formation of  -amyloid (A) plaques are associated with neuronal death in Alzheimer disease (AD). The plaque subtype Ax-42 occurs as an early event, with Ax-40 plaques forming at a later stage. In dementia with Lewy bodies (DLB), an increase in the amount of cortical A occurs without severe cortical neuronal losses.
Objective To advance our understanding of the natural history of A in neurodegenerative diseases.
Design We evaluated the expression of Ax-40 and Ax-42 in DLB using monoclonal antibodies and immunohistochemical techniques in 5 brain regions. The data were compared with those elicited with normal aging and from patients with AD.
Setting and Patients A postmortem study involving 19 patients with DLB without concurrent neuritic degeneration, 10 patients with AD, and 17 aged persons without dementia for control subjects.
Results The A plaques were more numerous in patients with DLB than in controls in most brain regions, although the Ax-42 plaque subtype was predominant in both conditions. Overall, Ax-42 plaque density was similar in patients with DLB and those with AD, but Ax-40 plaques were more numerous in persons with AD than in those with DLB. The ratio of Ax-40 to Ax-42 plaques was significantly reduced in persons with DLB compared with patients with AD.
Conclusions The A plaques were more numerous in patients with DLB than persons with normal aging, but the plaque subtypes were similar. The relative proportion of the 2 A plaque subtypes in DLB is distinguishable from that in AD.
From the Department of Neurology, MCP-Hahnemann University, Philadelphia, Pa (Dr Lippa); Department of Neuroscience, Osaka City University Medical School, Aebnoku, Japan (Drs Ozawa, Ishii, Arawaka, and Mori) Division of Molecular Pathology, Department of Pathological Sciences, University of Manchester, Manchester, England (Dr Mann); and Division of Neuropathology, Department of Pathology, University of Massachusetts Medical Center, Worcester (Dr Smith).
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