Amyloid-beta 42 Inhibitor Screening Service
Our Amyloid-beta 42 (Aβ42) inhibitor screening service provides efficient and accurate screening results, which are essential for the development of drugs for Alzheimer's disease (AD) and other neurodegenerative diseases. For further information regarding the products and services provided, project-specific consultation, and pricing, please submit an inquiry here.
Introduction
Distributed under Open Access license CC BY-SA 4.0, from Wiki,
without modification.
Aβ42 is a core component of AD pathology, and its excessive aggregation forms amyloid plaques, leading to neuronal damage and cognitive decline. The formation of Aβ42 is mainly through the action of β-secretase and γ-secretase. Therefore, inhibiting these enzymes or directly inhibiting the aggregation of Aβ42 is an important strategy for the treatment of AD. A variety of compounds, including small molecule inhibitors, peptide inhibitors, and antibodies, have demonstrated significant Aβ42 inhibitory effects in both in vitro and in vivo experiments.
Available Assays at Creative Biolabs
- High Throughput Screening of Aβ42 Inhibitors
The combination of bacterial culture and thioflavin T (ThT) fluorescent dye allows the real-time monitoring of Aβ42 aggregation within bacteria. This method quantifies the aggregation state of Aβ42 by observing changes in ThT fluorescence and enables rapid screening of potential anti-amyloid drugs.
By overexpressing the Aβ42 peptide in bacterial cells, its aggregation behavior in vivo can be simulated. The specific steps are as follows:
- Overexpression of Aβ42 peptide: The gene encoding Aβ42 is introduced into Escherichia coli (e.g. BL21 (DE3)) and the expression of Aβ42 peptide is induced by an inducible expression system (e.g. IPTG).
- Fluorescence Staining: The bacterial cells were stained with ThT dye, and then the aggregation phenomenon was observed under a fluorescence microscope. Aggregated Aβ42 formed amyloid-like fiber structures in the cells, which showed bright green fluorescence.
- Inhibitor Treatment: Potential inhibitors were co-incubated with Aβ42 peptides and then ThT was added for fluorescence detection. Inhibitors can reduce the aggregation of Aβ42, thereby reducing the fluorescence intensity of ThT.
- Quantitative Analysis: The degree of aggregation is assessed by measuring the change in ThT fluorescence intensity. For example, the inhibitory effect can be quantified by calculating the change in ThT fluorescence signal relative to the control group.
Fig.1 Screening small molecules that inhibit fibril formation using Escherichia coli.1
- Downstream Assays
We also offer a series of downstream tests to further verify the inhibitory activity of the screened compounds. When evaluating the inhibitory effect, it is necessary to ensure that the inhibitor is not toxic to bacterial cells. We offer cell viability assays. In addition to ThT fluorescence detection, SDS-PAGE and other techniques can be combined to further verify the aggregation state and inhibitory effect.
Fig.2 D737 rescues Aβ42 cytotoxicity in cells.1
Our Aβ42 inhibitor screening service delivers efficient and accurate screening results, providing substantial support for drug development for AD and other neurodegenerative diseases. We look forward to the opportunity to collaborate with you. Please contact us to discuss how our service can benefit your research.
Reference
- McKoy, Angela Fortner, et al. "A novel inhibitor of amyloid β (Aβ) peptide aggregation: from high throughput screening to efficacy in an animal model of Alzheimer disease." Journal of Biological Chemistry 287.46 (2012): 38992-39000. Distributed under Open Access license CC BY 4.0, without modification.
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