Mechanisms of Amyloid-Beta Peptide Uptake by Neurons: The Role of Lipid Rafts and Lipid Raft-Associated Proteins. (6th December 2010)

• Record Type: Journal Article
• Authors: Lai, Aaron Y.; McLaurin, JoAnne
• Other Names: Eckert Anne Academic Editor.
• Is Part Of: International journal of alzheimer's disease. Volume 2011(2011)
• Publication Date: 2010-12-06
• Subjects: Alzheimer's disease -- Periodicals; 616.831005
• DOI: 10.4061/2011/548380
• Languages: English
• ISSNs: 2090-8024

Abstract

Abstract : A hallmark pathological feature of Alzheimer's disease (AD) is the accumulation of extracellular plaques composed of the amyloid-beta (A β ) peptide. Thus, classically experiments were designed to examine A β toxicities within the central nervous system (CNS) from the extracellular space. However, a significant amount of evidence now suggests that intraneuronal accumulation of A β is neurotoxic and may play an important role in the disease progression of AD. One of the means by which neurons accumulate intracellular A β is through uptake of extracellular A β peptides, and this process may be a potential link between A β generation, synaptic dysfunction, and AD pathology. Recent studies have found that neuronal internalization of A β involves lipid rafts and various lipid raft-associated receptor proteins. Uptake mechanisms independent of lipid rafts have also been implicated. The aim of this paper is to summarize these findings and discuss their significance in the pathogenesis of AD.