Abstract
AbstractThe accumulation and deposition of β‐amyloid (Aβ) plaques in the brain is considered a potential pathogenic mechanism underlying Alzheimer's disease (AD). Chiral l/d‐FexCuySe nanoparticles (NPs) were fabricated that interfer with the self‐assembly of Aβ42 monomers and trigger the Aβ42 fibrils in dense structures to become looser monomers under 808 nm near‐infrared (NIR) illumination. d‐FexCuySe NPs have a much higher affinity for Aβ42 fibrils than l‐FexCuySe NPs and chiral Cu2−xSe NPs. The chiral FexCuySe NPs also generate more reactive oxygen species (ROS) than chiral Cu2−xSe NPs under NIR‐light irradiation. In living MN9D cells, d‐NPs attenuate the adhesion of Aβ42 to membranes and neuron loss after NIR treatment within 10 min without the photothermal effect. In‐vivo experiments showed that d‐FexCuySe NPs provide an efficient protection against neuronal damage induced by the deposition of Aβ42 and alleviate symptoms in a mouse model of AD, leading to the recovery of cognitive competence.
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