Abstract

Alzheimer's disease (AD) is an incurable chronic neurodegenerative disease. Until now, β-amyloid, mitochondrial viscosity and the relatively high concentration of hydrogen peroxide (H2O2) have been reported to be related with AD undergoing mutual interactions. In this work, a novel NIR fluorescent probe CBP was designed, synthesized and could be activated by H2O2 to release CBD, which was used to image β-amyloid fibrils in brain slices from transgenic mouse model and mitochondrial viscosity in living cells. CBP itself showed weak response towards β-amyloid and viscosity. However, upon exposure to H2O2, CBP was oxidized to the product CBD, which was accompanied with a slight fluorescence “turn-on” effect, attributing to the departure of the quenching group of the boronic acid pinacol ester. The resulting product CBP under H2O2 was highly responsive to the viscosity increase with a remarkable fluorescence enhancement at 635 nm by 53.5 folds, and simultaneously exhibited high specificity and selectivity towards Aβ1-42 aggregates with a fluorescence increase at 618 nm. Furthermore, CBP under H2O2 was applied in imaging β-amyloid fibrils in brain slices of AD transgenic mice and mitochondrial viscosity at the cellar level. Therefore, this novel NIR H2O2-activated fluorescent probe might serve as a dual imaging agent for β-amyloid fibrils and mitochondrial viscosity with low background, attributing to the H2O2-activation-induced fluorescence enhancements.

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