Heterotrimetallic Au@Cu₂Se nanozymes target inflamed neurons via suppression of oxidative stress and apoptosis to alleviate Alzheimer's disease.

ABSTRACT: Neuronal dysfunction mediated by oxidative stress and amyloid-β (Aβ) deposition is widely recognized as a core mechanism in the pathogenesis of Alzheimer's disease (AD). Aβ oligomers specifically interact with key mitochondrial proteins-such as alcohol dehydrogenase, cyclophilin D, and ATP synthase-markedly increasing reactive oxygen species (ROS) production, which leads to mitochondrial membrane potential collapse and disruption of energy metabolism. Although cuprous selenide and gold nanospheres can mimic the catalytic activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD), effectively scavenge excess ROS, restore mitochondrial membrane potential, and promote ATP synthesis through synergistic action, their therapeutic potential is limited by poor targeting specificity

SUBMITTER: Jing C 

PROVIDER: S-EPMC12741421 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature