Abstract
The 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-Fex Cuy Se 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-Fex Cuy Se NPs have a much higher affinity for Aβ42 fibrils than l-Fex Cuy Se NPs and chiral Cu2-x Se NPs. The chiral Fex Cuy Se NPs also generate more reactive oxygen species (ROS) than chiral Cu2-x Se 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-Fex Cuy Se 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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
