Targeting lncRNA NEAT1 Impedes Alzheimer’s Disease Progression via MicroRNA-193a Mediated CREB/BDNF and NRF2/NQO1 Pathways

Abstract Background Long noncoding RNA nuclear-enriched abundant transcript 1 (lnc-NEAT1) is closely implicated in neurological or degenerative diseases, while its implication AD rarely reported. This study aimed to investigate the effect of lnc-NEAT1 knockdown on neuron injury, inflammation, and oxidative stress AD, as well interaction with downstream targets pathways. Methods APPswe/PS1dE9 transgenic mice were injected negative control interference lentivirus. Besides, cellular model was constructed by amyloid β treatment primary cells; then, microRNA-193a (miR-193a) performed alone combination. Results In vivo experiments revealed that Lnc-NEAT1 improved cognition reflected Morrison water maze Y-maze assays. reduced injury apoptosis, decreased TNF-α IL-1β levels (indicating lower inflammation level), repressed ROS, MDA but promoted ATP SOD (suggesting activated CREB/BDNF NRF2/NQO1 pathways hippocampi mice. Notably, down-regulated miR-193a both vitro vivo; also, it acted a decoy miR-193a. showed apoptosis stress, cell viability, also model. Meanwhile, opposite effects, which attenuated knockdown-mediated reduction activation Conclusion reduces through activating mediated AD. Funding No