Dual Effect of Prussian Blue Nanoparticles on Aβ40 Aggregation: β-Sheet Fibril Reduction and Copper Dyshomeostasis Regulation

Alzheimer's disease (AD), affecting almost 50 million individuals worldwide, is currently the first cause of dementia. Despite the tremendous research efforts in the last decade, only four supportive or palliative drugs, namely, acetylcholinesterase (AChE) inhibitors donepezil, galantamine, and rivastigmine and the glutamate NMDA receptor antagonist memantine, are currently available. New therapeutic strategies are becoming prominent, such as the direct inhibition of amyloid formation or the regulation of metal homeostasis. In the present report, the potential use of Prussian blue (PB), a drug that is in the World Health Organization Model List of Essential Medicines, in AD treatment is demonstrated. Both in vitro and in cellulo studies indeed suggest that PB nanopartides (PBNPs) are capable of reducing the formation of typical amyloid-beta fibers (detected by thioflavin T fluorescence) and restoring the usual amyloid fibrillation pathway via chelation/sequestration of copper, which is found in high concentrations in senile plaques.

Automated summary

Alzheimer's disease, affecting nearly 50 million individuals globally, is currently the leading cause of dementia. Despite limited available drugs, new therapeutic strategies like direct inhibition of amyloid formation or metal homeostasis regulation are gaining prominence. Prussian blue, a drug listed in the World Health Organization Model List of Essential Medicines, shows potential in Alzheimer's disease treatment by reducing amyloid formation and restoring fibrillation pathways.