Systematic development of small molecules to inhibit specific microscopic steps of Aβ42 aggregation in Alzheimer's disease
(2017) In Proceedings of the National Academy of Sciences of the United States of America 114(2). p.200-208- Abstract
The aggregation of the 42-residue form of the amyloid-β peptide (Aβ42) 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 Aβ42 aggregation. Here, we exploit this approach to develop a rational drug discovery strategy against Aβ42 aggregation that uses as a readout the changes in the nucleation and elongation rate constants caused by candidate small molecules. We thus identify a pool of compounds that target specific microscopic steps in Aβ42 aggregation. We then test further these small molecules in human cerebrospinal fluid and in a Caenorhabditis elegans model of AD. Our results show that... (More)
The aggregation of the 42-residue form of the amyloid-β peptide (Aβ42) 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 Aβ42 aggregation. Here, we exploit this approach to develop a rational drug discovery strategy against Aβ42 aggregation that uses as a readout the changes in the nucleation and elongation rate constants caused by candidate small molecules. We thus identify a pool of compounds that target specific microscopic steps in Aβ42 aggregation. We then test further these small molecules in human cerebrospinal fluid and in a Caenorhabditis elegans model of AD. Our 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.
(Less)
- author
- organization
- publishing date
- 2017-01-10
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Alzheimer's disease, Amyloid-β peptide, Drug discovery, Protein aggregation, Protein misfolding
- in
- Proceedings of the National Academy of Sciences of the United States of America
- volume
- 114
- issue
- 2
- pages
- 200 - 208
- publisher
- National Academy of Sciences
- external identifiers
-
- scopus:85009348250
- pmid:28011763
- wos:000391439300012
- ISSN
- 0027-8424
- DOI
- 10.1073/pnas.1615613114
- language
- English
- LU publication?
- yes
- id
- 4c250a06-3b4f-49e1-80de-edad8cb6cbee
- date added to LUP
- 2017-02-28 14:45:30
- date last changed
- 2024-11-26 05:56:34
@article{4c250a06-3b4f-49e1-80de-edad8cb6cbee, abstract = {{<p>The aggregation of the 42-residue form of the amyloid-β peptide (Aβ42) 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 Aβ42 aggregation. Here, we exploit this approach to develop a rational drug discovery strategy against Aβ42 aggregation that uses as a readout the changes in the nucleation and elongation rate constants caused by candidate small molecules. We thus identify a pool of compounds that target specific microscopic steps in Aβ42 aggregation. We then test further these small molecules in human cerebrospinal fluid and in a Caenorhabditis elegans model of AD. Our 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.</p>}}, author = {{Habchi, Johnny and Chia, Sean and Limbocker, Ryan and Mannini, Benedetta and Ahn, Minkoo and Perni, Michele and Hansson, Oskar and Arosio, Paolo and Kumita, Janet R and Challa, Pavan Kumar and Cohen, Samuel I A and Linse, Sara and Dobson, Christopher M and Knowles, Tuomas P J and Vendruscolo, Michele}}, issn = {{0027-8424}}, keywords = {{Alzheimer's disease; Amyloid-β peptide; Drug discovery; Protein aggregation; Protein misfolding}}, language = {{eng}}, month = {{01}}, number = {{2}}, pages = {{200--208}}, publisher = {{National Academy of Sciences}}, series = {{Proceedings of the National Academy of Sciences of the United States of America}}, title = {{Systematic development of small molecules to inhibit specific microscopic steps of Aβ42 aggregation in Alzheimer's disease}}, url = {{http://dx.doi.org/10.1073/pnas.1615613114}}, doi = {{10.1073/pnas.1615613114}}, volume = {{114}}, year = {{2017}}, }