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Fluorescence-Based Monitoring of Early-Stage Aggregation of Amyloid-β, Amylin Peptide, Tau, and α-Synuclein Proteins

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Specialty Neurology
Date 2024 Aug 16
PMID 39150403
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Abstract

Early-stage aggregates of amyloid-forming proteins, specifically soluble oligomers, are implicated in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. Protein aggregation is typically monitored by fluorescence using the amyloid-binding fluorophore thioflavin T (ThT). Thioflavin T interacts, however, preferentially with fibrillar amyloid structures rather than with soluble, early-stage aggregates. In contrast, the two fluorophores, aminonaphthalene 2-cyanoacrylate-spiropyran (AN-SP) and triazole-containing boron-dipyrromethene (taBODIPY), were reported to bind preferentially to early-stage aggregates of amyloidogenic proteins. The present study compares ThT with AN-SP and taBODIPY with regard to their ability to monitor early stages of aggregation of four different amyloid-forming proteins, including amyloid-β (Aβ), tau protein, amylin, and α-synuclein. The results show that the three fluorophores vary in their suitability to monitor the early aggregation of different amyloid-forming proteins. For instance, in the presence of Aβ and amylin, the fluorescence intensity of AN-SP increased at an earlier stage of aggregation than the fluorescence of ThT, albeit with only a small fluorescence increase in the case of AN-SP. In contrast, in the presence of tau and amylin, the fluorescence intensity of taBODIPY increased at an earlier stage of aggregation than the fluorescence of ThT. Finally, α-synuclein aggregation could only be monitored by ThT fluorescence; neither AN-SP nor taBODIPY showed a significant increase in fluorescence over the course of aggregation of α-synuclein. These results demonstrate the ability of AN-SP and taBODIPY to monitor the formation of early-stage aggregates from specific amyloid-forming proteins at an early stage of aggregation, although moderate increases in fluorescence intensity, relatively large uncertainties in fluorescence values, and limited solubility of both fluorophores limit their usefulness for some amyloid proteins. The capability to monitor early aggregation of some amyloid proteins, such as amylin, might accelerate the discovery of aggregation inhibitors to minimize the formation of toxic oligomeric species for potential therapeutic use.

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References
1.
Cooper G, Leighton B, Dimitriadis G, Parry-Billings M, Kowalchuk J, Howland K . Amylin found in amyloid deposits in human type 2 diabetes mellitus may be a hormone that regulates glycogen metabolism in skeletal muscle. Proc Natl Acad Sci U S A. 1988; 85(20):7763-6. PMC: 282273. DOI: 10.1073/pnas.85.20.7763. View

2.
Bryan L, Awasthi S, Li Y, Nirmalraj P, Balog S, Yang J . Site-Specific C-Terminal Fluorescent Labeling of Tau Protein. ACS Omega. 2022; 7(50):47009-47014. PMC: 9773802. DOI: 10.1021/acsomega.2c06139. View

3.
Dzyuba S . BODIPY Dyes as Probes and Sensors to Study Amyloid-β-Related Processes. Biosensors (Basel). 2020; 10(12). PMC: 7760207. DOI: 10.3390/bios10120192. View

4.
Benilova I, Karran E, De Strooper B . The toxic Aβ oligomer and Alzheimer's disease: an emperor in need of clothes. Nat Neurosci. 2012; 15(3):349-57. DOI: 10.1038/nn.3028. View

5.
Raleigh D, Zhang X, Hastoy B, Clark A . The β-cell assassin: IAPP cytotoxicity. J Mol Endocrinol. 2017; 59(3):R121-R140. DOI: 10.1530/JME-17-0105. View