Beta amyloid plaque

Beta amyloid plaques. [Image courtesy of NIH]

An international team of researchers has identified a technique that uses fluoride nanoparticles to potentially eliminate protein deformations. The method, which also can promote positive structural changes, could lead to the prevention and treatment of Alzheimer’s disease.

The scientists from Tokyo University of Science (TUS) in Japan and Nazarbayev University in Kazakhstan published the research in ACS Applied Bio Materials.

Noting the amyloid fibrils formed with the self-assembly of denatured proteins are associated with Alzheimer’s disease, the researchers discovered that fluoride nanoparticles could alter the assembly and structure of the amyloid β protein.

Fluoride nanoparticles are used in in vivo imaging, including brain imaging applications.

In particular, the scientists reported the influence of fluoride nanoparticles and surrounding ions on the development of β-sheet structure in amyloid β proteins.

Aberrations in the protein secondary structures or assembly are associated with neurodegenerative diseases, including Alzheimer’s.

The ACS Applied Bio Materials study used a solution of fluoride ceramic (CeF3) nanoparticles to investigate a section of amyloid β peptide.

Using Fourier transform infrared spectroscopy, the scientists discovered that peptides close to the nanoparticle surface were more likely to form β-sheets.

The researchers also analyzed the use of other surrounding ions in the solution. “What we found was very surprising. Even without the nanoparticles, the environment affected the rate of secondary structure formation,” said Masakazu Umezawa, a TUS professor, in a news release. “This effect, resulting from a combination of electrostatic interaction and hydrogen bonding, was exaggerated upon adding nanoparticles.” Umezawa says that the careful selection of ions and nanoparticles can either suppress or promote β-sheet formation. “This implies that the process can be controlled and engineered to eradicate adverse effects,” he added.

The research community has remained divided concerning the etiology of Alzheimer’s disease. The consensus view in recent decades is the so-called amyloid hypothesis, which assumes the buildup of amyloid-β is the primary cause of Alzheimer’s disease. However, many drug candidates targeting the peptide have failed to deliver convincing results in Alzheimer’s patients.