Title

ABeta Aggregation and Possible Implications in Alzheimer's Disease Pathogenesis.

Document Type

Journal Article

Publisher

Wiley-Blackwell

Faculty

Computing, Health and Science

School

Exercise, Biomedical and Health Science, Centre for Alzheimer's Disease

RAS ID

9008

Comments

This article was originally published as: Bharadwaj, P. , Dubey, A., Masters, C., Martins, R. N., & Macreadie, I. (2009). ABeta aggregation and possible implications in Alzheimer's disease pathogenesis. Journal of Cellular and Molecular Medicine, 13(3), 412-421. Original article available here

Abstract

Amyloid β protein (Aβ) has been associated with Alzheimer's disease (AD) because it is a major component of the extracellular plaque found in AD brains. Increased Aβ levels correlate with the cognitive decline observed in AD. Sporadic AD cases are thought to be chiefly associated with lack of Aβ clearance from the brain, unlike familial AD which shows increased Aβ production. Aβ aggregation leading to deposition is an essential event in AD. However, the factors involved in Aβ aggregation and accumulation in sporadic AD have not been completely characterized. This review summarizes studies that have examined the factors that affect Aβ aggregation and toxicity. By necessity these are studies that are performed with recombinant-derived or chemically synthesized Aβ. 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 Aβ toxicity. An understanding of Aβ oligomerization may lead to better strategies to prevent AD.