Abstract
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
Current Alzheimer Research
Title: Protection Mechanisms Against Aβ42 Aggregation
Volume: 5 Issue: 6
Author(s): Y. Yan and C. Wang
Affiliation:
Keywords: Amyloid-β peptide (Aβ), Alzheimer's disease (AD), protection, Aβ42 aggregation, Aβ40, NMR, heat shock protein, L-PGDS, heme, methionine oxidation
Abstract: 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.
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Cite this article as:
Yan Y. and Wang C., Protection Mechanisms Against Aβ42 Aggregation, Current Alzheimer Research 2008; 5 (6) . https://dx.doi.org/10.2174/156720508786898460
DOI https://dx.doi.org/10.2174/156720508786898460 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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