Protection Mechanisms Against Aβ42 Aggregation
- Authors: Yilin Yan, Christopher Connors, Chunyu Wang3
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View Affiliations Hide Affiliations3 Biology Department, Rensselear Polytechnic Institute, Troy, NY 12180, USA
- Source: Advances in Alzheimer's Research Volume 1 , pp 47-64
- Publication Date: November 2013
- Language: English
Protection Mechanisms Against Aβ42 Aggregation, Page 1 of 1
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It is widely accepted that Aβ42 aggregation is a central event in the pathogenesis of Alzheimer's 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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