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Issue 977 coverALZHEIMER'S DISEASE: VASCULAR ETIOLOGY AND PATHOLOGY Copyright © 2002 by the New York Academy of Sciences
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Articles by FRIEDLAND, R. P.
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Articles by FRIEDLAND, R. P.
Annals of the New York Academy of Sciences 977:387-390 (2002)
© 2002 New York Academy of Sciences

Lipid Metabolism, Epidemiology, and the Mechanisms of Alzheimer's Disease

ROBERT P. FRIEDLAND

Laboratory of Neurogeriatrics, Department of Neurology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA

Address for correspondence: Robert P. Friedland, M.D., Laboratory of Neurogeriatrics, Department of Neurology, Case Western Reserve University School of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106. Voice: 216-368-1912; fax: 216-368-1989.
rpf2{at}po.cwru.edu
Ann. N.Y. Acad. Sci. 977: 387-390 (2002).

Global variations in the incidence and prevalence of Alzheimer's disease (AD) have not been explained. Patterns of dietary intake of fats and other nutrients may be partly responsible. Recent work with transgenic mice overexpressing the ß-amyloid precursor protein suggests that anti-Aß antibodies enhance clearance of the Aß protein from the brain and reduce plaque burden. This has been shown even with anti-Aß antibodies that do not enter the brain. Many factors other than circulating anti-Aß antibodies may influence this important process of Aß clearance, including the Aß-binding elements, apolipoproteins E and J, circulating LDL, HDL, and LRP, alpha-2-macroglobulin, and transthyretin. Also important may be clearance of antibody-antigen complexes from the circulation, as well as complement, metals, and estrogen. Dietary intake of lipids may influence the ability of Aß-binding proteins to enhance clearance of Aß from the brain to blood. Understanding processes of Aß clearance from brain may aid in determining the causes of AD in individuals, as well as the causes of global variations in incidence and prevalence of the disease.

Key Words: platelets • LRP • estrogen • complement • alpha-2-macroglobulin • metals • apolipoprotein E • apolipoprotein J




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