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Systematic development of small molecules against Aβ aggregation

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The aggregation of the 42-residue form of the amyloid-beta peptide (Abeta42) is a pivotal event in Alzheimer’s disease (AD). The use of chemical kinetics has recently enabled highly accurate quantifications of the effects of small molecules on specific microscopic steps in Abeta42 aggregation. I will explain how we have exploited this approach to develop a rational drug discovery strategy against Abeta42 aggregation that uses as a read-out the changes in the nucleation and elongation rate constants caused by candidate small molecules. We have thus identified a pool of compounds that target specific microscopic steps in Abeta42 aggregation. We have then tested further these small molecules in human cerebrospinal fluid and in a Caenorhabditis elegans model of AD. These results show that this strategy represents a powerful approach to identify systematically small molecule lead compounds, thus offering an appealing opportunity to reduce the attrition problem in drug discovery.

This talk is part of the Biological and Statistical Physics discussion group (BSDG) series.

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