Abeta aggregation and possible implications in Alzheimer's disease pathogenesis

Bharadwaj, P, Dubey, A, Masters, C, Martins, R and Macreadie, I 2009, 'Abeta aggregation and possible implications in Alzheimer's disease pathogenesis', Journal of Cellular and Molecular Medicine, vol. 13, no. 3, pp. 412-421.

Document type: Journal Article
Collection: Journal Articles

Title Abeta aggregation and possible implications in Alzheimer's disease pathogenesis
Author(s) Bharadwaj, P
Dubey, A
Masters, C
Martins, R
Macreadie, I
Year 2009
Journal name Journal of Cellular and Molecular Medicine
Volume number 13
Issue number 3
Start page 412
End page 421
Total pages 10
Publisher Wiley-Blackwell Publishing Ltd.
Abstract Amyloid beta protein (Abeta) has been associated with Alzheimer's disease (AD) because it is a major component of the extracellular plaque found in AD brains. Increased Abeta levels correlate with the cognitive decline observed in AD. Sporadic AD cases are thought to be chiefly associated with lack of Abeta clearance from the brain, unlike familial AD which shows increased Abeta production. Abeta aggregation leading to deposition is an essential event in AD. However, the factors involved in Abeta aggregation and accumulation in sporadic AD have not been completely characterized. This review summarizes studies that have examined the factors that affect Abeta aggregation and toxicity. By necessity these are studies that are performed with recombinant-derived or chemically synthesized Abeta. The studies therefore are not done in animals but in cell culture, which includes neuronal cells, other mammalian cells and, in some cases, non-mammalian cells that also appear susceptible to Abeta toxicity. An understanding of Abeta oligomerization may lead to better strategies to prevent AD.
Subject Biochemistry and Cell Biology not elsewhere classified
Keyword(s) Alzheimer's disease
peptide toxicity
DOI - identifier 10.1111/j.1582-4934.2009.00609.x
Copyright notice © 2009 John Wiley & Sons, Inc
ISSN 1582-1838
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