Author(s): Yin F, Liu J, Ji X, Wang Y, Zidichouski J,
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Abstract Alzheimer's disease (AD) is a common form of neurodegenerative disease. Mounting evidence suggests that metal ions play a key role in the aggregation of amyloid β peptide (Aβ), which acts as a factor or cofactor in the etiopathogenesis of AD. Therefore, inhibition of Aβ aggregation emerges as a potential approach for the treatment of AD. We have found that baicalin can interact with copper directly and inhibits Aβ1-42 aggregation. In addition, baicalin protects SH-SY5Y cells from oxidative injuries induced by Aβ1-42 aggregation through decreasing H(2)O(2) production that is normally formed as a deleterious by-product of beta amyloid aggregation and the formation of plaques. Taken together, these data indicate that baicalin may be a potential agent to inhibit Aβ aggregation and thereby delay, mitigate or modify the progression of neurodegenerative diseases such as AD. Crown Copyright © 2011. Published by Elsevier Ireland Ltd. All rights reserved.
This article was published in Neurosci Lett
and referenced in Medicinal chemistry