Protection Mechanisms Against Aβ42 Aggregation

Author(s): Y. Yan, C. Wang

Journal Name: Current Alzheimer Research

Volume 5 , Issue 6 , 2008

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It is widely accepted that Aβ42 aggregation is a central event in the pathogenesis of Alzheimers disease. Aβ42 oligomers and fibrils cause the breakdown of neural circuits, neuronal death and eventually dementia. There are a number of physiological molecules that can protect Aβ42 from aggregation. Promoting such protective molecules and mechanisms against Aβ42 aggregation may be a novel direction in AD drug discovery. One of the most striking protective molecules is none other than Aβ40, which inhibits Aβ42 aggregation in a specific and dosage dependent manner. Aβ40 is a critical, built-in mechanism against Aβ42 aggregation. A number of other molecules and mechanisms also inhibit Aβ42 aggregation, such as heat shock proteins, L-PGDS, heme and methionine oxidation. The relevance of these protective mechanisms to AD pathogenesis and intervention is discussed.

Keywords: Amyloid-β peptide (Aβ), Alzheimer's disease (AD), protection, Aβ42 aggregation, Aβ40, NMR, heat shock protein, L-PGDS, heme, methionine oxidation

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Article Details

Year: 2008
Page: [548 - 554]
Pages: 7
DOI: 10.2174/156720508786898460
Price: $65

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